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Joseph Caprioli - One of the best experts on this subject based on the ideXlab platform.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    Abstract The expression of alpha (αA and αB) and Beta (βA1/A3, βA2, βA4, and βB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (αA, αB, βA1/A3, βA4, and βB2 approximately 50% and βA2 ~ 40%) and protein (αA ~ 50%, αB ~ 63%, βA1/A3 ~ 70%, and βB2 ~ 38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (αA, αB, and βB2 approximately 37% and βA1/A3 ~ 70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    The expression of alpha (alphaA and alphaB) and Beta (BetaA1/A3, BetaA2, BetaA4, and BetaB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (alphaA, alphaB, BetaA1/A3, BetaA4, and BetaB2 approximately 50% and BetaA2~40%) and protein (alphaA~50%, alphaB~63%, BetaA1/A3~70%, and BetaB2~38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (alphaA, alphaB, and BetaB2 approximately 37% and BetaA1/A3~70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

Natik Piri - One of the best experts on this subject based on the ideXlab platform.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    Abstract The expression of alpha (αA and αB) and Beta (βA1/A3, βA2, βA4, and βB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (αA, αB, βA1/A3, βA4, and βB2 approximately 50% and βA2 ~ 40%) and protein (αA ~ 50%, αB ~ 63%, βA1/A3 ~ 70%, and βB2 ~ 38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (αA, αB, and βB2 approximately 37% and βA1/A3 ~ 70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    The expression of alpha (alphaA and alphaB) and Beta (BetaA1/A3, BetaA2, BetaA4, and BetaB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (alphaA, alphaB, BetaA1/A3, BetaA4, and BetaB2 approximately 50% and BetaA2~40%) and protein (alphaA~50%, alphaB~63%, BetaA1/A3~70%, and BetaB2~38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (alphaA, alphaB, and BetaB2 approximately 37% and BetaA1/A3~70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

M Song - One of the best experts on this subject based on the ideXlab platform.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    Abstract The expression of alpha (αA and αB) and Beta (βA1/A3, βA2, βA4, and βB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (αA, αB, βA1/A3, βA4, and βB2 approximately 50% and βA2 ~ 40%) and protein (αA ~ 50%, αB ~ 63%, βA1/A3 ~ 70%, and βB2 ~ 38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (αA, αB, and βB2 approximately 37% and βA1/A3 ~ 70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    The expression of alpha (alphaA and alphaB) and Beta (BetaA1/A3, BetaA2, BetaA4, and BetaB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (alphaA, alphaB, BetaA1/A3, BetaA4, and BetaB2 approximately 50% and BetaA2~40%) and protein (alphaA~50%, alphaB~63%, BetaA1/A3~70%, and BetaB2~38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (alphaA, alphaB, and BetaB2 approximately 37% and BetaA1/A3~70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

Jacky M K Kwong - One of the best experts on this subject based on the ideXlab platform.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    Abstract The expression of alpha (αA and αB) and Beta (βA1/A3, βA2, βA4, and βB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (αA, αB, βA1/A3, βA4, and βB2 approximately 50% and βA2 ~ 40%) and protein (αA ~ 50%, αB ~ 63%, βA1/A3 ~ 70%, and βB2 ~ 38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (αA, αB, and βB2 approximately 37% and βA1/A3 ~ 70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

  • modulation of alpha and Beta Crystallin expression in rat retinas with ocular hypertension induced ganglion cell degeneration
    Brain Research, 2007
    Co-Authors: Natik Piri, M Song, Jacky M K Kwong, Joseph Caprioli
    Abstract:

    The expression of alpha (alphaA and alphaB) and Beta (BetaA1/A3, BetaA2, BetaA4, and BetaB2) Crystallin genes were analyzed at the mRNA and protein levels in rat retinas with ocular hypertension-induced ganglion cell death. An animal model with progressive loss of retinal ganglion cells (RGC) was generated by elevation of intraocular pressure (IOP). The estimated RGC loss was approximately 8% and 20% at 2 and 5 weeks post IOP elevation, respectively. mRNA and protein quantification showed that alpha and Beta Crystallin genes were downregulated at both transcriptional (alphaA, alphaB, BetaA1/A3, BetaA4, and BetaB2 approximately 50% and BetaA2~40%) and protein (alphaA~50%, alphaB~63%, BetaA1/A3~70%, and BetaB2~38%) levels 2 weeks after IOP elevation. In experimental retinas 5 weeks after IOP elevation, the levels of Crystallin mRNAs were higher than at 2 weeks and were comparable to that of control retinas. However, the levels of the corresponding proteins were still lower (alphaA, alphaB, and BetaB2 approximately 37% and BetaA1/A3~70%) than in control retinas. Furthermore, we found that the expression of these genes in the retina is predominantly localized to the cells in the GCL and to a lesser degree in the INL and ONL. Colocalization of the Crystallin-positive and Fluorogold retrogradely labeled cells indicated that the cells expressing alpha and Beta Crystallins in the GCL are RGCs. In summary, we showed that alpha and Beta Crystallins are expressed in the retina predominantly by RGCs and that their expression is affected by ocular hypertension.

Theo J M Hulsebos - One of the best experts on this subject based on the ideXlab platform.

  • assignment of the Beta b1 Crystallin gene crybb1 to human chromosome 22 and mouse chromosome 5
    Genomics, 1995
    Co-Authors: Theo J M Hulsebos, D J Gilbert, Olivier Delattre, L J Smink, Ian Dunham, A Westerveld, Gilles Thomas, Nancy A Jenkins, Neal G Copeland
    Abstract:

    By using primers complementary to the rat {Beta}B1 Crystallin gene sequence, we amplified exons 5 and 6 of the orthologous human gene (CRYBB1). The amplified human segments displayed greater than 88% sequence homology to the corresponding rat and bovine sequences. CRYBB1 was assigned to the group 5 region in 22q11.2-q12.1 by hybridizing the exon 6 PCR product to somatic cell hybrids containing defined portions of human chromosome 22. The exon 5 and exon 6 PCR products of CRYBB1 were used to localize, by interspecific backcross mapping, the mouse gene (Crybb1) to the central portion of chromosome 5. Three other {Beta} Crystallin genes ({Beta}B2(-l), {Beta}B3, and {Beta}A4) have previously been mapped to the same regions in human and mouse. We demonstrate that the {Beta}B1 and {Beta}A4 Crystallin genes are very closely linked in the two species. These assignments complete the mapping and identification of the human and mouse homologues of the major {Beta} Crystallins genes that are expressed in the bovine lens. 39 refs., 5 figs., 1 tab.

  • assignment of the Beta b1 Crystallin gene crybb1 to human chromosome 22 and mouse chromosome 5
    Genomics, 1995
    Co-Authors: Theo J M Hulsebos, D J Gilbert, Olivier Delattre, L J Smink, Ian Dunham, A Westerveld, Gilles Thomas, Nancy A Jenkins, Neal G Copeland
    Abstract:

    By using primers complementary to the rat Beta B1 Crystallin gene sequence, we amplified exons 5 and 6 of the orthologous human gene (CRYBB1). The amplified human segments displayed greater than 88% sequence homology to the corresponding rat and bovine sequences. CRYBB1 was assigned to the group 5 region in 22q11.2-q12.1 by hybridizing the exon 6 PCR product to somatic cell hybrids containing defined portions of human chromosome 22. The exon 5 and exon 6 PCR products of CRYBB1 were used to localize, by interspecific backcross mapping, the mouse gene (Crybb1) to the central portion of chromosome 5. Three other Beta Crystallin genes (Beta B2(-1), Beta B3, and Beta A4) have previously been mapped to the same regions in human and mouse. We demonstrate that the Beta B1 and Beta A4 Crystallin genes are very closely linked in the two species. These assignments complete the mapping and identification of the human and mouse homologues of the major Beta Crystallins genes that are expressed in the bovine lens.

  • regional fine mapping of the Beta Crystallin genes on chromosome 22 excludes these genes as physically linked markers for neurofibromatosis type 2
    Genes Chromosomes and Cancer, 1993
    Co-Authors: E K Bijlsma, Olivier Delattre, A Westerveld, Gilles Thomas, Jenneke A Juyn, Thomas Melot, Jan P Dumanski, Theo J M Hulsebos
    Abstract:

    Neurofibromatosis type 2 (NF2) is a rare autosomal dominant disease, characterized by the development of bilateral vestibular schwannomas. The NF2 gene has been assigned to chromosome 22. Cataract and other eye abnormalities are frequently seen in NF2 patients. The specific association of eye abnormalities and NF2 might be caused by a genetic change on chromosome 22 that affects both the NF2 gene and a physically linked Crystallin gene. In order to test this hypothesis, we regionally localized the known Crystallin genes (i.e. CRYBB2, CRYBB2P1, CRYBB3, and CRYBA4) on chromosome 22. Crystallin gene-specific probes were hybridized to an extended panel of human x rodent somatic cell hybrids containing various portions of chromosome 22. It was found that all Crystallin genes map to a very small region on chromosome 22 that is physically separate from the NF2 gene region by at least 160 kb of DNA. In addition, we found that the βB Crystallin genes (CRYBB2, CRYBB2P1, and CRYBB3) are clustered on a 300 kb Sacll fragment and that the βA4 Crystallin gene (CRYBA4) is not part of this cluster. We conclude that the ocular manifestations in many NF2 patients are probably not the primary consequence of rearrangements on chromosome 22 that involve both the NF2 gene and a nearby β Crystallin gene.\\wiley5\wiley$\Wiley-JWPH\final\jwph471