Vascular Lesion

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Eugene Y Chen - One of the best experts on this subject based on the ideXlab platform.

  • peroxisome proliferator activated receptor γ coactivator 1β pgc 1β protein attenuates Vascular Lesion formation by inhibition of chromatin loading of minichromosome maintenance complex in smooth muscle cells
    Journal of Biological Chemistry, 2013
    Co-Authors: Jifeng Zhang, Lin Chang, Eugene Y Chen
    Abstract:

    Abstract Proliferation of Vascular smooth muscle cells (VSMCs) in response to Vascular injury plays a critical role in Vascular Lesion formation. Emerging data suggest that peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) is a key regulator of energy metabolism and other biological processes. However, the physiological role of PGC-1β in VSMCs remains unknown. A decrease in PGC-1β expression was observed in balloon-injured rat carotid arteries. PGC-1β overexpression substantially inhibited neointima formation in vivo and markedly inhibited VSMC proliferation and induced cell cycle arrest at the G1/S transition phase in vitro. Accordingly, overexpression of PGC-1β decreased the expression of minichromosome maintenance 4 (MCM4), which leads to a decreased loading of the MCM complex onto chromatin at the replication origins and decreased cyclin D1 levels, whereas PGC-1β loss of function by adenovirus containing PGC-1β shRNA resulted in the opposite effect. The transcription factor AP-1 was involved in the down-regulation of MCM4 expression. Furthermore, PGC-1β is up-regulated by metformin, and metformin-associated anti-proliferative activity in VSMCs is at least partially dependent on PGC-1β. Our data show that PGC-1β is a critical component in regulating DNA replication, VSMC proliferation, and Vascular Lesion formation, suggesting that PGC-1β may emerge as a novel therapeutic target for control of proliferative Vascular diseases.

  • peroxisome proliferator activated receptor γ coactivator 1β pgc 1β protein attenuates Vascular Lesion formation by inhibition of chromatin loading of minichromosome maintenance complex in smooth muscle cells
    Journal of Biological Chemistry, 2013
    Co-Authors: Yanhong Guo, Jifeng Zhang, Lin Chang, Yanbo Fan, Jiandie D Lin, Eugene Y Chen
    Abstract:

    Proliferation of Vascular smooth muscle cells (VSMCs) in response to Vascular injury plays a critical role in Vascular Lesion formation. Emerging data suggest that peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) is a key regulator of energy metabolism and other biological processes. However, the physiological role of PGC-1β in VSMCs remains unknown. A decrease in PGC-1β expression was observed in balloon-injured rat carotid arteries. PGC-1β overexpression substantially inhibited neointima formation in vivo and markedly inhibited VSMC proliferation and induced cell cycle arrest at the G1/S transition phase in vitro. Accordingly, overexpression of PGC-1β decreased the expression of minichromosome maintenance 4 (MCM4), which leads to a decreased loading of the MCM complex onto chromatin at the replication origins and decreased cyclin D1 levels, whereas PGC-1β loss of function by adenovirus containing PGC-1β shRNA resulted in the opposite effect. The transcription factor AP-1 was involved in the down-regulation of MCM4 expression. Furthermore, PGC-1β is up-regulated by metformin, and metformin-associated anti-proliferative activity in VSMCs is at least partially dependent on PGC-1β. Our data show that PGC-1β is a critical component in regulating DNA replication, VSMC proliferation, and Vascular Lesion formation, suggesting that PGC-1β may emerge as a novel therapeutic target for control of proliferative Vascular diseases. Background: Peroxisome proliferator-activated receptor γ coactivator 1β (PGC-1β) is a key regulator of biological processes. Results: Overexpression of PGC-1β inhibits neointima formation and Vascular smooth muscle cell proliferation. Conclusion: PGC-1β inhibits proliferation through impaired minichromosome maintenance (MCM) complex loading onto chromatin. Significance: PGC-1β may emerge as an important therapeutic target relevant for the treatment of proliferative Vascular disorders.

Christopher D M Fletcher - One of the best experts on this subject based on the ideXlab platform.

  • composite hemangioendothelioma a complex low grade Vascular Lesion mimicking angiosarcoma
    The American Journal of Surgical Pathology, 2000
    Co-Authors: Simon Nayler, Eduardo Calonje, Brian P Rubin, John K C Chan, Christopher D M Fletcher
    Abstract:

    Eight cases of a previously uncharacterized Vascular neoplasm, showing varying combinations of benign, low-grade malignant, and malignant Vascular components are described. Seven tumors occurred in the dermis and/or subcutis and one occurred in the oral submucosa. The patients were all adults with a median age of 39.5 years (range, 21-71 years). Five patients were men. The tumors arose predominantly in the hands and feet, and the Lesions were usually of several years duration. The tumors were composed of a complex admixture of histologic components that varied from tumor to tumor, such that no two tumors looked precisely the same. This was due to variation in the proportions of each component as well as the manner in which each component was distributed throughout each Lesion. The predominant histologic components were epithelioid hemangioendothelioma (HE) and retiform HE, which were each present in seven of the tumors. Areas of spindle cell HE were identified in four Lesions. Angiosarcoma-like elements were identified in seven tumors. One of the tumors was associated with an arteriovenous malformation and one was associated with an area of lymphangioma circumscriptum. Of six cases with follow up (median duration, 6.5 years), three have recurred locally and, to date, only one has metastasized. We think composite HE is best regarded as a low-grade malignant Vascular neoplasm, and the available data suggest that it behaves more favorably than conventional angiosarcoma. The existence of these composite Lesions has led to careful reexamination of the concept of HE. The term HE, in that it is currently synonymous with a low-grade malignant Vascular tumor, should be reserved for Lesions that have true metastatic potential, albeit with low frequency.

  • hobnail hemangioma a pseudomalignant Vascular Lesion with a reappraisal of targetoid hemosiderotic hemangioma
    The American Journal of Surgical Pathology, 1999
    Co-Authors: Louis Guillou, Eduardo Calonje, Paul Speight, Juan Rosai, Christopher D M Fletcher
    Abstract:

    The clinicopathologic features of 15 cutanous hemangiomas having a distinctive and frequently pseudomalignant morphologic appearance are presented. There were 5 male and 9 female patients, whose ages at diagnosis ranged from 11 to 58 years (median 30.5). An angiomatous/pigmented, nontargetoid, flat, or exophytic Lesion of variable duration was the main presenting sign. The tumor sizes ranged from 0.4 cm to 2 cm (median 1 cm). The locations included the lower limb, particularly the thigh (8); the trunk, including the shoulder area (4); the head (1); the gingiva (1); and the tongue (1). One patient had two Lesions; none had a concomitant Vascular anomaly or was suspected to have HIV infection. Treatment consisted of excisional biopsy in all cases. Follow-up information on 10 patients (range 4-66 months; median 13 months) showed no recurrence. On microscopic examination, the Lesion showed a biphasic pattern characterized by the presence of well-formed, dilated, Vascular channels in superficial dermis and a collagen-dissecting, pseudoangiosarcomatous pattern as the Lesion infiltrated deeper into the dermis. The lining endothelium consistently showed distinctive hobnail cytomorphology; although there were endoluminal stromal papillae, there was no endothelial multilayering or tufting. Cytologic atypia was minimal or absent, and there were no mitoses. In 3 cases, the morphologic features were reminiscent of retiform hemangioendothelioma. Immunohistochemistry performed in 8 cases showed variable reactivity of endothelial cells with CD31, CD34, Factor VIII-related antigen, and Ulex europaeus agglutinin-1 in all cases; smooth muscle actin-positive pericytes were observed focally around some of the abnormal Vascular spaces. The above-described hemangiomatous Lesions share many features with so-called targetoid hemosiderotic hemangioma (a clinically descriptive term), but show a variable, often minimal, amount of hemosiderin deposition. The histologically descriptive term hobnail hemangioma is proposed to designate these Lesions. Hobnail hemangioma should be distinguished from well-differentiated angiosarcoma, patch-stage Kaposi's sarcoma, and retiform hemangioendothelioma, with which it may be confused.

Jifeng Zhang - One of the best experts on this subject based on the ideXlab platform.

  • peroxisome proliferator activated receptor γ coactivator 1β pgc 1β protein attenuates Vascular Lesion formation by inhibition of chromatin loading of minichromosome maintenance complex in smooth muscle cells
    Journal of Biological Chemistry, 2013
    Co-Authors: Jifeng Zhang, Lin Chang, Eugene Y Chen
    Abstract:

    Abstract Proliferation of Vascular smooth muscle cells (VSMCs) in response to Vascular injury plays a critical role in Vascular Lesion formation. Emerging data suggest that peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) is a key regulator of energy metabolism and other biological processes. However, the physiological role of PGC-1β in VSMCs remains unknown. A decrease in PGC-1β expression was observed in balloon-injured rat carotid arteries. PGC-1β overexpression substantially inhibited neointima formation in vivo and markedly inhibited VSMC proliferation and induced cell cycle arrest at the G1/S transition phase in vitro. Accordingly, overexpression of PGC-1β decreased the expression of minichromosome maintenance 4 (MCM4), which leads to a decreased loading of the MCM complex onto chromatin at the replication origins and decreased cyclin D1 levels, whereas PGC-1β loss of function by adenovirus containing PGC-1β shRNA resulted in the opposite effect. The transcription factor AP-1 was involved in the down-regulation of MCM4 expression. Furthermore, PGC-1β is up-regulated by metformin, and metformin-associated anti-proliferative activity in VSMCs is at least partially dependent on PGC-1β. Our data show that PGC-1β is a critical component in regulating DNA replication, VSMC proliferation, and Vascular Lesion formation, suggesting that PGC-1β may emerge as a novel therapeutic target for control of proliferative Vascular diseases.

  • peroxisome proliferator activated receptor γ coactivator 1β pgc 1β protein attenuates Vascular Lesion formation by inhibition of chromatin loading of minichromosome maintenance complex in smooth muscle cells
    Journal of Biological Chemistry, 2013
    Co-Authors: Yanhong Guo, Jifeng Zhang, Lin Chang, Yanbo Fan, Jiandie D Lin, Eugene Y Chen
    Abstract:

    Proliferation of Vascular smooth muscle cells (VSMCs) in response to Vascular injury plays a critical role in Vascular Lesion formation. Emerging data suggest that peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) is a key regulator of energy metabolism and other biological processes. However, the physiological role of PGC-1β in VSMCs remains unknown. A decrease in PGC-1β expression was observed in balloon-injured rat carotid arteries. PGC-1β overexpression substantially inhibited neointima formation in vivo and markedly inhibited VSMC proliferation and induced cell cycle arrest at the G1/S transition phase in vitro. Accordingly, overexpression of PGC-1β decreased the expression of minichromosome maintenance 4 (MCM4), which leads to a decreased loading of the MCM complex onto chromatin at the replication origins and decreased cyclin D1 levels, whereas PGC-1β loss of function by adenovirus containing PGC-1β shRNA resulted in the opposite effect. The transcription factor AP-1 was involved in the down-regulation of MCM4 expression. Furthermore, PGC-1β is up-regulated by metformin, and metformin-associated anti-proliferative activity in VSMCs is at least partially dependent on PGC-1β. Our data show that PGC-1β is a critical component in regulating DNA replication, VSMC proliferation, and Vascular Lesion formation, suggesting that PGC-1β may emerge as a novel therapeutic target for control of proliferative Vascular diseases. Background: Peroxisome proliferator-activated receptor γ coactivator 1β (PGC-1β) is a key regulator of biological processes. Results: Overexpression of PGC-1β inhibits neointima formation and Vascular smooth muscle cell proliferation. Conclusion: PGC-1β inhibits proliferation through impaired minichromosome maintenance (MCM) complex loading onto chromatin. Significance: PGC-1β may emerge as an important therapeutic target relevant for the treatment of proliferative Vascular disorders.

Myles L Pensak - One of the best experts on this subject based on the ideXlab platform.

  • intraVascular papillary endothelial hyperplasia of the internal auditory canal
    Laryngoscope, 2012
    Co-Authors: Gordon H Sun, Nael Shoman, Philip V Theodosopoulos, Ady Kendler, Myles L Pensak
    Abstract:

    IntraVascular papillary endothelial hyperplasia (IPEH), also known as Masson's tumor, is a rare Vascular Lesion characterized by intraVascular proliferation of endothelial-lined papillae and a propensity for manifestation in the head and neck. Signs and symptoms associated with IPEH generally occur due to compressive effects of the Lesion on adjacent structures. A rare instance of IPEH occurring in the internal auditory canal is presented herein. Clinical presentation, radiographic and pathologic findings, and management strategies are discussed.

Seungo Ko - One of the best experts on this subject based on the ideXlab platform.

  • utility of sodium tetradecyl sulfate sclerotherapy from benign oral Vascular Lesion
    Maxillofacial plastic and reconstructive surgery, 2016
    Co-Authors: Boeun Choi, Dae Ho Leem, Jina Baek, Seungo Ko
    Abstract:

    Hemangioma and Vascular malformation are benign Vascular Lesions that often occur in cephalic and cervical region. Currently, surgical resection, laser therapy, angiographic embolization, use of steroids, and sclerotherapy are used as treatments. This study reports three cases of benign Vascular Lesions that are remarkably treated by sodium tetradecyl sulfate (STS) injection, of which occurred in oral cavity and around the mouth. Three percent of STS was diluted with 0.9 % of normal saline, and it was injected to the Lesion site at least once. The result of treatment was evaluated based on clinical findings. Surgical treatment of hemangioma and Vascular malformation occurred in oral cavity is not normally used because of esthetic issues and potential hemorrhage. On the other hand, sclerotherapy using STS is an effective therapy compare to surgical treatment. Despite the number of STS injection was different for each patient, all three patients had reached satisfactory level through the treatment with gradual diminution of Lesions.