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Shuwei Chen - One of the best experts on this subject based on the ideXlab platform.
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Abstract 5171: TFAP2B overexpression contributes to tumor growth & progression of thyroid cancer through AKT&VEGF/PEDF signaling pathway
Tumor Biology, 2018Co-Authors: Zhongyuan Yang, Shuwei ChenAbstract:TFAP2 is a family of transcription factors implicated in many aspects of development.TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating thyroid carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on thyroid cancer growth & identified the underlying mechanisms of actions in thyroid cancer cells.We examined the expression of TFAP2B in thyroid cancer cell lines & tumor tissues. We also analyzed the TNM staging of TFAP2B in thyroid cancer. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated thyroid cancer cell growth, angiogenesis & apoptosis, & further confirmed the role of TFAP2B in tumor growth in a thyroid cancerxenograft mouse model.TFAP2B was expressed in thyroid cancer lines t 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5171.
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abstract 5171 TFAP2B overexpression contributes to tumor growth progression of thyroid cancer through akt vegf pedf signaling pathway
Cancer Research, 2018Co-Authors: Zhongyuan Yang, Shuwei ChenAbstract:TFAP2 is a family of transcription factors implicated in many aspects of development.TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating thyroid carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on thyroid cancer growth & identified the underlying mechanisms of actions in thyroid cancer cells.We examined the expression of TFAP2B in thyroid cancer cell lines & tumor tissues. We also analyzed the TNM staging of TFAP2B in thyroid cancer. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated thyroid cancer cell growth, angiogenesis & apoptosis, & further confirmed the role of TFAP2B in tumor growth in a thyroid cancerxenograft mouse model.TFAP2B was expressed in thyroid cancer lines t 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5171.
Zhongyuan Yang - One of the best experts on this subject based on the ideXlab platform.
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TFAP2B overexpression contributes to tumor growth and progression of thyroid cancer through the COX-2 signaling pathway.
Cell death & disease, 2019Co-Authors: Huayong Zhang, Zhongyuan Yang, Dingbo Shi, Zhipeng Chen, Tianrun Liu, Weichao Chen, Fan Yao, Wuguo DengAbstract:Thyroid cancer is commonly seen in the clinic with a rapidly increasing incidence globally. COX-2 overexpression correlates with the pathologic type of thyroid carcinoma, and it has been suggested that COX-2 overexpression is associated with a poor prognosis. However, little is known about its upstream regulatory mechanism. Bioinformatics suggested that transcription factor AP-2 beta (TFAP2B) might specifically bind to the COX-2 promoter, which was confirmed by biotin-labeled COX-2 promoter pulldown and luciferase reporter assays. We performed western blot and immunohistochemical staining to detect the expression of TFAP2B/COX-2 in thyroid cancer tissues (T) and the matched adjacent noncarcinoma tissues (ANT), and investigated the relationship between TFAP2B/COX-2 expression and clinical pathological factors in thyroid cancer patients. Afterward, MTS, colony formation, cell-apoptosis assay, transwell-invasion and scratch assays were performed to examine the proliferation, apoptosis, invasion, and migration of thyroid cancer cells with TFAP2B knocked down or overexpressed. The mouse xenograft experiment was performed to study in vivo the proliferation of thyroid cancer cells with TFAP2B knocked down or overexpressed. We found that TFAP2B bound to the promoter of COX-2 to activate its expression. Western blot and immunohistochemistry showed that TFAP2B/COX-2 was highly expressed in thyroid cancer, and high TFAP2B and COX-2 expression was associated with aggressive clinicopathological features in thyroid cancer. TFAP2B mediated thyroid cancer cell proliferation, apoptosis, invasion, and migration via the COX-2 signaling pathway in vitro and in vivo. TFAP2B bound to the promoter of COX-2 to activate its expression, indicating that TFAP2B is a critical regulatory molecule in the COX-2 signaling pathway that promoted tumor progression in thyroid cancer.
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Abstract 5171: TFAP2B overexpression contributes to tumor growth & progression of thyroid cancer through AKT&VEGF/PEDF signaling pathway
Tumor Biology, 2018Co-Authors: Zhongyuan Yang, Shuwei ChenAbstract:TFAP2 is a family of transcription factors implicated in many aspects of development.TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating thyroid carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on thyroid cancer growth & identified the underlying mechanisms of actions in thyroid cancer cells.We examined the expression of TFAP2B in thyroid cancer cell lines & tumor tissues. We also analyzed the TNM staging of TFAP2B in thyroid cancer. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated thyroid cancer cell growth, angiogenesis & apoptosis, & further confirmed the role of TFAP2B in tumor growth in a thyroid cancerxenograft mouse model.TFAP2B was expressed in thyroid cancer lines t 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5171.
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abstract 5171 TFAP2B overexpression contributes to tumor growth progression of thyroid cancer through akt vegf pedf signaling pathway
Cancer Research, 2018Co-Authors: Zhongyuan Yang, Shuwei ChenAbstract:TFAP2 is a family of transcription factors implicated in many aspects of development.TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating thyroid carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on thyroid cancer growth & identified the underlying mechanisms of actions in thyroid cancer cells.We examined the expression of TFAP2B in thyroid cancer cell lines & tumor tissues. We also analyzed the TNM staging of TFAP2B in thyroid cancer. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated thyroid cancer cell growth, angiogenesis & apoptosis, & further confirmed the role of TFAP2B in tumor growth in a thyroid cancerxenograft mouse model.TFAP2B was expressed in thyroid cancer lines t 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5171.
Dingbo Shi - One of the best experts on this subject based on the ideXlab platform.
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TFAP2B overexpression contributes to tumor growth and progression of thyroid cancer through the COX-2 signaling pathway.
Cell death & disease, 2019Co-Authors: Huayong Zhang, Zhongyuan Yang, Dingbo Shi, Zhipeng Chen, Tianrun Liu, Weichao Chen, Fan Yao, Wuguo DengAbstract:Thyroid cancer is commonly seen in the clinic with a rapidly increasing incidence globally. COX-2 overexpression correlates with the pathologic type of thyroid carcinoma, and it has been suggested that COX-2 overexpression is associated with a poor prognosis. However, little is known about its upstream regulatory mechanism. Bioinformatics suggested that transcription factor AP-2 beta (TFAP2B) might specifically bind to the COX-2 promoter, which was confirmed by biotin-labeled COX-2 promoter pulldown and luciferase reporter assays. We performed western blot and immunohistochemical staining to detect the expression of TFAP2B/COX-2 in thyroid cancer tissues (T) and the matched adjacent noncarcinoma tissues (ANT), and investigated the relationship between TFAP2B/COX-2 expression and clinical pathological factors in thyroid cancer patients. Afterward, MTS, colony formation, cell-apoptosis assay, transwell-invasion and scratch assays were performed to examine the proliferation, apoptosis, invasion, and migration of thyroid cancer cells with TFAP2B knocked down or overexpressed. The mouse xenograft experiment was performed to study in vivo the proliferation of thyroid cancer cells with TFAP2B knocked down or overexpressed. We found that TFAP2B bound to the promoter of COX-2 to activate its expression. Western blot and immunohistochemistry showed that TFAP2B/COX-2 was highly expressed in thyroid cancer, and high TFAP2B and COX-2 expression was associated with aggressive clinicopathological features in thyroid cancer. TFAP2B mediated thyroid cancer cell proliferation, apoptosis, invasion, and migration via the COX-2 signaling pathway in vitro and in vivo. TFAP2B bound to the promoter of COX-2 to activate its expression, indicating that TFAP2B is a critical regulatory molecule in the COX-2 signaling pathway that promoted tumor progression in thyroid cancer.
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TFAP2B overexpression contributes to tumor growth and a poor prognosis of human lung adenocarcinoma through modulation of ERK and VEGF/PEDF signaling
Molecular cancer, 2014Co-Authors: Ke Shi, Jingshu Wang, Wangbing Chen, Dingbo Shi, Yun Tian, Wei Guo, Xiangsheng Xiao, Tiebang KangAbstract:Background: TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on lung adenocarcinomas growth and identified the underlying mechanisms of actions in non-small cell lung cancer (NSCLC) cells. Methods: We first examined the expression of TFAP2B in lung cancer cell lines and tumor tissues. We also analyzed the prognostic predicting value of TFAP2B in lung adenocarcinomas. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated lung cancer cell growth, angiogenesis and apoptosis, and further confirmed the role of TFAP2B in tumor growth in a lung cancer xenograft mouse model. Results: TFAP2B was highly expressed in NSCLC cell lines and tumor tissues. Strong TFAP2B expression showed a positive correlation with the poor prognoses of patients with lung adenocarcinomas (P< 0.001). TFAP2B knockdown by siRNA significantly inhibited cell growth and induced apoptosis in NSCLC cells in vitro and in a lung cancer subcutaneous xenograft model, whereas TFAP2B overexpression promoted cell growth. The observed regulation of cell growth was accompanied by the TFAP2B-mediated modulation of the ERK/p38, caspase/cytochrome-c and VEGF/PEDF-dependent signaling pathways in NSCLC cells. Conclusions: These results indicate that TFAP2B plays a critical role in regulating lung adenocarcinomas growth and could serve as a promising therapeutic target for lung cancer treatment.
Sergey Bruskin - One of the best experts on this subject based on the ideXlab platform.
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Integrated computational approach to the analysis of RNA-seq data reveals new transcriptional regulators of psoriasis
Experimental & Molecular Medicine, 2016Co-Authors: Alena Zolotarenko, Evgeny Chekalin, Alexandre Mesentsev, Ludmila Kiseleva, Elena Gribanova, Rohini Mehta, Ancha Baranova, Tatiana V Tatarinova, Eleonora S Piruzian, Sergey BruskinAbstract:Psoriasis is a common inflammatory skin disease with complex etiology and chronic progression. To provide novel insights into the regulatory molecular mechanisms of the disease, we performed RNA sequencing analysis of 14 pairs of skin samples collected from patients with psoriasis. Subsequent pathway analysis and extraction of the transcriptional regulators governing psoriasis-associated pathways was executed using a combination of the MetaCore Interactome enrichment tool and the cisExpress algorithm, followed by comparison to a set of previously described psoriasis response elements. A comparative approach allowed us to identify 42 core transcriptional regulators of the disease associated with inflammation (NFκB, IRF9, JUN, FOS, SRF), the activity of T cells in psoriatic lesions (STAT6, FOXP3, NFATC2, GATA3, TCF7, RUNX1), the hyperproliferation and migration of keratinocytes (JUN, FOS, NFIB, TFAP2A, TFAP2C) and lipid metabolism (TFAP2, RARA, VDR). In addition to the core regulators, we identified 38 transcription factors previously not associated with the disease that can clarify the pathogenesis of psoriasis. To illustrate these findings, we analyzed the regulatory role of one of the identified transcription factors (TFs), FOXA1. Using ChIP-seq and RNA-seq data, we concluded that the atypical expression of the FOXA1 TF is an important player in the disease as it inhibits the maturation of naive T cells into the ( CD4+FOXA1+CD47+CD69+PD-L1(hi)FOXP3− ) regulatory T cell subpopulation, therefore contributing to the development of psoriatic skin lesions. Highly sensitive genetic sequencing has uncovered genes and regulatory elements that may play key roles in the development of psoriasis. Little is known about the exact reasons of the manifestation of skin disease psoriasis, although it appears to be triggered by abnormal immune cell signalling. It can also cause systemic inflammation resulting in serious heart conditions and strokes. Sergey Bruskin together with scientists across Russia and the US, carried out RNA sequencing on samples from the skin lesions and healthy skin of 14 Caucasian patients. Using comparative bioinformatic approach The team identified 38 novel transcriptional regulators previously unassociated with psoriasis, and dissected 42 proteins to be the main governors of the disease. One of the novel transcription regulators, the protein known as FOXA1, appears to inhibit the maturation of regulatory immune cells, triggering abnormal immune cell signalling.
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Integrated computational approach to the analysis of RNA-seq data reveals new transcriptional regulators of psoriasis
Experimental & Molecular Medicine, 2016Co-Authors: Alena Zolotarenko, Evgeny Chekalin, Alexandre Mesentsev, Ludmila Kiseleva, Elena Gribanova, Rohini Mehta, Ancha Baranova, Tatiana V Tatarinova, Eleonora S Piruzian, Sergey BruskinAbstract:Highly sensitive genetic sequencing has uncovered genes and regulatory elements that may play key roles in the development of psoriasis. Little is known about the exact reasons of the manifestation of skin disease psoriasis, although it appears to be triggered by abnormal immune cell signalling. It can also cause systemic inflammation resulting in serious heart conditions and strokes. Sergey Bruskin together with scientists across Russia and the US, carried out RNA sequencing on samples from the skin lesions and healthy skin of 14 Caucasian patients. Using comparative bioinformatic approach The team identified 38 novel transcriptional regulators previously unassociated with psoriasis, and dissected 42 proteins to be the main governors of the disease. One of the novel transcription regulators, the protein known as FOXA1, appears to inhibit the maturation of regulatory immune cells, triggering abnormal immune cell signalling. Psoriasis is a common inflammatory skin disease with complex etiology and chronic progression. To provide novel insights into the regulatory molecular mechanisms of the disease, we performed RNA sequencing analysis of 14 pairs of skin samples collected from patients with psoriasis. Subsequent pathway analysis and extraction of the transcriptional regulators governing psoriasis-associated pathways was executed using a combination of the MetaCore Interactome enrichment tool and the cisExpress algorithm, followed by comparison to a set of previously described psoriasis response elements. A comparative approach allowed us to identify 42 core transcriptional regulators of the disease associated with inflammation (NFκB, IRF9, JUN, FOS, SRF), the activity of T cells in psoriatic lesions (STAT6, FOXP3, NFATC2, GATA3, TCF7, RUNX1), the hyperproliferation and migration of keratinocytes (JUN, FOS, NFIB, TFAP2A, TFAP2C) and lipid metabolism (TFAP2, RARA, VDR). In addition to the core regulators, we identified 38 transcription factors previously not associated with the disease that can clarify the pathogenesis of psoriasis. To illustrate these findings, we analyzed the regulatory role of one of the identified transcription factors (TFs), FOXA1. Using ChIP-seq and RNA-seq data, we concluded that the atypical expression of the FOXA1 TF is an important player in the disease as it inhibits the maturation of naive T cells into the ( CD4+FOXA1+CD47+CD69+PD-L1(hi)FOXP3− ) regulatory T cell subpopulation, therefore contributing to the development of psoriatic skin lesions.
Trevor Williams - One of the best experts on this subject based on the ideXlab platform.
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Progressive Loss of Retinal Ganglion Cells in Activating Protein-2β Neural Crest Cell KO Mice.
Current eye research, 2021Co-Authors: Aftab Taiyab, Trevor Williams, Monica Akula, Paula Deschamps, Alexander K Ball, Anthony Saraco, Judith A. West-maysAbstract:PURPOSE Our lab has shown that conditionally disrupting the transcription factor activating protein 2β (TFAP2B) gene, responsible for the activating protein-2β (AP-2β) transcription factor, exclusively in cranial neural crest cells (AP-2β NCC KO), leads to anterior segment dysgenesis and a closed angle phenotype. The purpose of the current study is to determine if there is a progressive loss of retinal ganglion cells (RGCs) in the mutant over time and whether this loss was associated with macroglial activity changes and elevated intraocular pressure (IOP). METHODS Using the Cre-loxP system, we generated a conditional knockout of TFAP2B exclusively in cranial NCC (AP-2β NCC KO). Immunohistochemistry was performed using anti-Brn3a, anti-GFAP and anti-Vimentin antibodies. IOP was measured using a Tonometer and the data was analyzed using GraphPad Prism software. Brn3a and DAPI positive cells were counted using Image-J and statistical analysis was performed with GraphPad Prism software. RESULTS Our findings revealed that while no statistical difference in Brn3a expression was observed between wild-type and mutant mice at postnatal day (P) 4 or P10, at P40 (p
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Anomalous incisor morphology indicates tissue-specific roles for Tfap2a and TFAP2B in tooth development.
Developmental biology, 2021Co-Authors: Emily D. Woodruff, Eric Van Otterloo, Galaxy C. Gutierrez, Trevor Williams, Martin J. CohnAbstract:Mice possess two types of teeth that differ in their cusp patterns; incisors have one cusp and molars have multiple cusps. The patterning of these two types of teeth relies on fine-tuning of the reciprocal molecular signaling between dental epithelial and mesenchymal tissues during embryonic development. The AP-2 transcription factors, particularly Tfap2a and TFAP2B, are essential components of such epithelial-mesenchymal signaling interactions that coordinate craniofacial development in mice and other vertebrates, but little is known about their roles in the regulation of tooth development and shape. Here we demonstrate that incisors and molars differ in their temporal and spatial expression of Tfap2a and TFAP2B. At the bud stage, Tfap2a is expressed in both the epithelium and mesenchyme of the incisors and molars, but TFAP2B expression is restricted to the molar mesenchyme, only later appearing in the incisor epithelium. Tissue-specific deletions show that loss of the epithelial domain of Tfap2a and TFAP2B affects the number and spatial arrangement of the incisors, notably resulting in duplicated lower incisors. In contrast, deletion of these two genes in the mesenchymal domain has little effect on tooth development. Collectively these results implicate epithelial expression of Tfap2a and TFAP2B in regulating the extent of the dental lamina associated with patterning the incisors and suggest that these genes contribute to morphological differences between anterior (incisor) and posterior (molar) teeth within the mammalian dentition.
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Anomalous incisor morphology indicates tissue-specific roles for Tfap2a and TFAP2B in tooth development
2020Co-Authors: Emily D. Woodruff, Eric Van Otterloo, Galaxy C. Gutierrez, Trevor Williams, Martin J. CohnAbstract:Mice possess two types of teeth that differ in their cusp patterns; incisors have one cusp and molars have multiple cusps. The patterning of these two types of teeth relies on fine-tuning of the reciprocal molecular signaling between dental epithelial and mesenchymal tissues during embryonic development. Here we show that the incisors are populated only at early time points by the neural crest, whereas the molars continue to receive contributions at later stages, revealing a temporal difference that could alter epithelial-mesenchymal signaling dynamics between these two types of teeth. The AP-2 transcription factors, particularly Tfap2a and TFAP2B, are essential components of such epithelial-mesenchymal signaling interactions that coordinate craniofacial development in mice and other mammals, but little is known about their roles in the regulation of tooth development and shape. We demonstrate that incisors and molars differ in their temporal and spatial expression of Tfap2a and TFAP2B; in particular, at the bud stage, Tfap2a is expressed in both the epithelium and mesenchyme of the incisors and molars but expression of TFAP2B is restricted to the mesenchyme of the molars. Tissue-specific deletions show that loss of the epithelial domain of Tfap2a and TFAP2B affects the number and spatial arrangement of the incisors, notably resulting in duplicated lower incisors. In contrast, deletion of these two genes in the mesenchymal domain has little effect on tooth development. Collectively these results implicate epithelial expression of Tfap2a and TFAP2B in dorsal-ventral patterning of the incisors and suggest that these genes contribute to morphological differences between anterior (incisor) and posterior (molar) teeth within the mammalian dentition. HighlightsO_LILate-migrating cranial neural crest cells contribute extensively to the developing molar tooth germs but minimally to the incisors. C_LIO_LIDuring tooth development, transcription factors Tfap2a and TFAP2B are expressed in spatially and temporally dynamic patterns and differ between incisor and molar tooth germs. C_LIO_LIEpithelial expression of Tfap2a and TFAP2B is necessary for incisor development, but mesenchymal expression of these genes is not required. C_LI
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ap 2β is required for formation of the murine trabecular meshwork and schlemm s canal
Experimental Eye Research, 2020Co-Authors: Monica Akula, Trevor Williams, Aftab Taiyab, Paula Deschamps, Shannin Yee, Alexander K Ball, Judith A WestmaysAbstract:Abstract Previously, we have shown that TFAP2B, the gene encoding transcription factor AP-2β, is needed for normal mouse eye development. Specifically, targeted loss of TFAP2B in neural crest cells (NCCs)1 and their derivatives, particularly the periocular mesenchyme (POM), resulted in anterior segment defects affecting the cornea and angle tissue. These defects were further associated with an increase in intraocular pressure (IOP). The present study investigates the underlying changes in embryonic and postnatal POM cell development and differentiation caused by loss of AP-2β in the NCCs, particularly in the structures that control aqueous outflow, using Wnt1Cre+/-; TFAP2B-/lox; tdTomatolox/+ mice (AP-2β neural crest cell knockout or AP-2β NCC KO). Toluidine blue-stained sections and ultrathin sections stained with uranyl acetate and lead citrate were used to assess morphology and ultrastructure, respectively. Immunohistochemistry of KO and control eyes was performed at embryonic day (E) 15.5, E18.5, postnatal day (P) 1, P7 and P14 using phospho-histone H3 (PH3), α-smooth muscle actin (α-SMA), myocilin and endomucin antibodies, as well as a TUNEL assay. Conditional deletion of AP-2β in the NCC-derived POM resulted in defects that appeared during both embryogenesis and postnatal stages. Fate mapping of the knockout cells in the mutants revealed that the POM migrated appropriately into the eye during embryogenesis. However, during postnatal stages a significant reduction in POM proliferation in the angle region was observed in the mutants compared to controls. This was accompanied by a lack of expression of appropriate trabecular meshwork and Schlemm's canal markers. This is the first study to show that AP-2β is required for development and differentiation of the trabecular meshwork and Schlemm's canal. Together, these defects likely contributed to the elevated intraocular pressure (IOP) previously reported in the AP-2β NCC KO mice.
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AP-2β Is a Downstream Effector of PITX2 Required to Specify Endothelium and Establish Angiogenic Privilege During Corneal Development.
Investigative ophthalmology & visual science, 2016Co-Authors: Lisheng Chen, Trevor Williams, Judith A. West-mays, Vanessa Martino, Alan A. Dombkowski, Philip J. GageAbstract:Purpose The homeodomain transcription factor, PITX2, is at the apex of a genetic pathway required for corneal development, but the critical effector genes regulated by the PITX2 remain unknown. The purpose of this study was to discover and validate PITX2-dependent mechanisms required for specifying cell lineages and establishing angiogenic privilege within the developing cornea. Methods Microarrays were used to compare gene expression in corneas isolated from temporal Pitx2 knockout embryos and control littermates. Quantitative RT-PCR and immunohistochemistry was used to further validate TFAP2B expression differences in Pitx2 knockout versus control corneas. In situ hybridization and protein immunohistochemistry were used to assay eyes of a TFAP2B allelic series of embryos to identify differentiated cellular lineages in the cornea, blood vessel endothelium, or lymphatic vessel endothelium. Results We show that PITX2 is required for the expression of TFAP2B, encoding the AP-2β transcription factor, in the neural crest during corneal development. Markers of differentiated corneal epithelium and stroma are expressed in the absence of AP-2β. In contrast, markers of differentiated corneal endothelium are not expressed in the absence of AP-2β. Endomucin+ blood vessels are present throughout the developing corneal stroma in the absence of AP-2β, whereas LYVE1+ lymphatic vessels are not found. Conclusions The AP-2β transcription factor is an important effector of PITX2 function during corneal development, required for differentiation of corneal endothelium and establishment of angiogenic privilege. Unlike PITX2, AP-2β is not required for the early expression of available lineage specific markers for the corneal epithelium and stroma during embryogenesis, nor establishment of lymphangiogenic privilege. Therefore, additional PITX2-dependent factors likely regulate these latter processes during embryonic development. These results extend our understanding of the genetic mechanisms regulating cornea development.