Zobrazeno 1 - 10
of 18
pro vyhledávání: '"Daniel T. Meehan"'
Autor:
Gina Samuelson, Ruth M. Gill, Celia Jenkinson, Duane Delimont, Radko Komers, Jared J. Hartsock, Grady Phillips, Dominic Cosgrove, Michael Anne Gratton, James Hasson, Daniel T. Meehan, Brianna Dufek
Publikováno v:
Nephrology Dialysis Transplantation. 35
Background and Aims In Alport syndrome (AS), endothelin type A receptor (ETAR) activation plays a role in both renal and inner ear pathologies. Currently, angiotensin converting enzyme inhibitors or angiotensin II type 1 receptor (AT1R) blockers are
Autor:
Grady Phillips, Daniel T. Meehan, Marisa Zallocchi, Michael Anne Gratton, Duane Delimont, Dominic Cosgrove, Brianna Dufek
Publikováno v:
Hearing Research. 341:100-108
Alport syndrome, a type IV collagen disorder, manifests as glomerular disease associated with hearing loss with thickening of the glomerular and strial capillary basement membranes (SCBMs). We have identified a role for endothelin-1 (ET-1) activation
Autor:
Shiguang Liu, Duane Delimont, Brianna Dufek, Michael Anne Gratton, Linda Cheung, Wenping Song, Grady Phillips, Daniel T. Meehan, Dominic Cosgrove
Publikováno v:
Kidney International. 90:300-310
Recent work demonstrates that Alport glomerular disease is mediated through a biomechanical strain-sensitive activation of mesangial actin dynamics. This occurs through a Rac1/CDC42 cross-talk mechanism that results in the invasion of the subcapillar
Autor:
Grady Phillips, Michael Anne Gratton, Duane Delimont, Deidre A. MacKenna, Gretchen Bain, Dominic Cosgrove, Daniel T. Meehan, Brianna Dufek, Michael Hartnett, Gina Samuelson
Publikováno v:
Kidney Int
Lysyl oxidase like-2 (LOXL2) is an amine oxidase with both intracellular and extracellular functions. Extracellularly, LOXL2 promotes collagen and elastin crosslinking, whereas intracellularly, LOXL2 has been reported to modify histone H3, stabilize
Publikováno v:
The American Journal of Pathology. 183(4):1269-1280
Alport syndrome, hereditary glomerulonephritis with hearing loss, results from mutations in type IV collagen COL4A3, COL4A4, or COL4A5 genes. The mechanism for delayed glomerular disease onset is unknown. Comparative analysis of Alport mice and CD151
Autor:
Richard M. Tempero, Duane Delimont, Velidi H. Rao, Daniel T. Meehan, Kathyrn D. Rodgers, Marisa Zallocchi, Xiwu Chen, Ambra Pozzi, Dominic Cosgrove
Publikováno v:
The American Journal of Pathology. 172:761-773
Previous work has shown that integrin α1-null Alport mice exhibit attenuated glomerular disease with decreased matrix accumulation and live much longer than strain-matched Alport mice. However, the mechanism underlying this observation is unknown. H
Publikováno v:
The American Journal of Pathology. 166:1465-1474
Alport syndrome results from mutations in genes encoding collagen α3(IV), α4(IV), or α5(IV) and is characterized by progressive glomerular disease associated with a high-frequency sensorineural hearing loss. Earlier studies of a gene knockout mous
Autor:
Clifford E. Kashtan, Gautam Bhattacharya, Duane Delimont, Dominic Cosgrove, George E. Lees, Rakesh K. Singh, Brian R. Berridge, Daniel T. Meehan, Velidi H. Rao
Publikováno v:
Pediatric Nephrology. 20:732-739
Matrix metalloproteinases (MMPs) play an important regulatory role in many biological and pathological processes and their specific role in Alport syndrome (AS) is not yet clearly defined. In this study, the naturally occurring canine X-linked AS was
Autor:
George E. Lees, Rakesh K. Singh, Ryochi Nemori, Kathyrn D. Rodgers, Velidi H. Rao, Dominic Cosgrove, Clifford E. Kashtan, Gautam Bhattacharya, Brian R. Berridge, Daniel T. Meehan
Publikováno v:
Kidney International. 63(5):1736-1748
Increased expression of MMP-2, MMP-9 (type IV collagenases/gelatinases), and MT1-MMP in canine X-linked Alport syndrome (XLAS). Background Alport syndrome is a group of genetic disorders resulting from mutations in either the α3(IV), α4(IV) or α5(
Autor:
Sarah Ryan, Victor Koteliansky, Velidi H. Rao, Philip Gotwals, Nicole Fager, Ryoichi Nemori, Daniel T. Meehan, Dominic Cosgrove, Kathyrn D. Rodgers
Publikováno v:
Kidney International. 63:1338-1355
Monocytes may promote myofibroblast accumulation and apoptosis in Alport renal fibrosis. Background In interstitial fibrosis, monocytes and myofibroblasts have been directly implicated in scarring, apoptosis, and tissue necrosis. While much has been