Ischemic acute renal failure: Long-term histology of cell and matrix changes in the rat

Forbes, Josephine M.; Hewitson, Tim D.; Becker, Gavin J.; Jones, Colin L.

doi:10.1046/j.1523-1755.2000.00097.x

Cited by 153 publications

(136 citation statements)

References 27 publications

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“…In the early days after unilateral renal I/R injury, nevertheless, active cell proliferation is observed in the interstitial area and the tubular compartment. 42 In addition, there is evidence that postischemic interstitial cells are regulated independently by mediators such as growth factors. 43 Interstitial fibroblasts respond shortly to acute ischemic insult, and could contribute to interstitial pathology during an acute phase.…”

Section: Discussionmentioning

confidence: 99%

Cytoglobin, a Novel Member of the Globin Family, Protects Kidney Fibroblasts against Oxidative Stress under Ischemic Conditions

Nishi

Inagi

Kawada

et al. 2011

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 99%

Cytoglobin, a Novel Member of the Globin Family, Protects Kidney Fibroblasts against Oxidative Stress under Ischemic Conditions

Nishi

Inagi

Kawada

et al. 2011

The American Journal of Pathology

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“…It has been reported that significant accumulation of type IV collagen occurs in an ischemic injury model (8). MMP-2 and MMP-9 are reportedly upregulated in the tubulointerstitial space (2) or in the endothelial compartment of the kidney after renal ischemia (6).…”

Section: Discussionmentioning

confidence: 99%

Enhancement of in vitro human tubulogenesis by endothelial cell-derived factors: implications for in vivo tubular regeneration after injury

Miya¹,

Maeshima²,

Mishima³

et al. 2011

American Journal of Physiology-Renal Physiology

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“…Ten animals per group were counted. Results were expressed as proportional area of positive staining (28).…”

Section: Immunohistochemistry For Renal CMLmentioning

confidence: 99%

Modulation of Soluble Receptor for Advanced Glycation End Products by Angiotensin-Converting Enzyme-1 Inhibition in Diabetic Nephropathy

Forbes¹,

Thorpe²,

Thallas‐Bonke³

et al. 2005

Journal of the American Society of Nephrology

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195

129

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Recent studies have identified that first-line renoprotective agents that interrupt the renin-angiotensin system not only reduce BP but also can attenuate advanced glycation end product (AGE) accumulation. This study used in vitro, preclinical, and human approaches to explore the potential effects of these agents on the modulation of the receptor for AGE (RAGE). Bovine aortic endothelial cells that were exposed to the angiotensin-converting enzyme inhibitor (ACEi) ramiprilat in the presence of high glucose demonstrated a significant increase in soluble RAGE (sRAGE) secreted into the medium. In streptozotocininduced diabetic rats, ramipril treatment (ACEi) at 3 mg/L for 24 wk reduced the accumulation of skin collagen-linked carboxymethyllysine and pentosidine, as well as circulating and renal AGE. Renal gene upregulation of total RAGE (all three splice variants) was observed in ACEi-treated animals. There was a specific increase in the gene expression of the splice variant C-truncated RAGE (sRAGE). There were also increases in sRAGE protein identified within renal cells with ACEi treatment, which showed AGE-binding ability. This was associated with decreases in renal full-length RAGE protein from ACEi-treated rats. Decreases in plasma soluble RAGE that were significantly increased by ACEi treatment were also identified in diabetic rats. Similarly, there was a significant increase in plasma sRAGE in patients who had type 1 diabetes and were treated with the ACEi perindopril. Complexes between sRAGE and carboxymethyllysine were identified in human and rodent diabetic plasma. It is postulated that ACE inhibition reduces the accumulation of AGE in diabetes partly by increasing the production and secretion of sRAGE into plasma.

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Ischemic acute renal failure: Long-term histology of cell and matrix changes in the rat

Cited by 153 publications

References 27 publications

Cytoglobin, a Novel Member of the Globin Family, Protects Kidney Fibroblasts against Oxidative Stress under Ischemic Conditions

Cytoglobin, a Novel Member of the Globin Family, Protects Kidney Fibroblasts against Oxidative Stress under Ischemic Conditions

Enhancement of in vitro human tubulogenesis by endothelial cell-derived factors: implications for in vivo tubular regeneration after injury

Modulation of Soluble Receptor for Advanced Glycation End Products by Angiotensin-Converting Enzyme-1 Inhibition in Diabetic Nephropathy

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