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Monocytes may promote myofibroblast accumulation and apoptosis in Alport renal fibrosis11See Editorial by Nikolic-Paterson, p. 1582. by Rodgers, Kathyrn D.; Rao, Velidi; Meehan, Daniel T.; Fager, Nicole; Gotwals, Philip; Ryan, Sarah T.; Koteliansky, Victor; Nemori, Ryoichi; Cosgrove, Dominic is a Medicine article available to read on EtoBox.
## Background: In interstitial fibrosis, monocytes and myofibroblasts have been directly implicated in scarring, apoptosis, and tissue necrosis. while much has been done to explore the role of these cell types individually in fibrosis, the interactive dependency of monocytes and myofibroblasts has been only marginally explored. ## Methods: Alport mice were treated or not with a soluble receptor inhibitor for transforming growth factor-beta 1 (tgf-beta 1), which was previously shown to inhibit the accumulation of myofibroblasts, but not monocytes, in the tubulointerstitium. kidneys were examined for fibrosis using several matrix markers, tgf-beta 1 mrna expression by in situ hybridization, apoptosis using the terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick end labeling (tunel) assay, expression of matrix metalloproteinases (mmps) and tissue inhibitors of metalloproteinases (timps) by dual immunofluorescence microscopy, mmp activity by gelatin and in situ zymography, mmp mrna expression by reverse transcription-polymerase chain reaction (rt-pcr), and basement membrane degradation by dual immunofluorescence confocal microscopy and electron microscopy. ## Resul
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- Author
- Rodgers, Kathyrn D.; Rao, Velidi; Meehan, Daniel T.; Fager, Nicole; Gotwals, Philip; Ryan, Sarah T.; Koteliansky, Victor; Nemori, Ryoichi; Cosgrove, Dominic
- Publisher
- Nature Publishing Group; Elsevier ; Elsevier Inc.; Elsevier BV; ScienceOpen (ISSN 0085-2538)
- Published
- 2003
- Language
- EN
- Field
- Medicine (Health Sciences)