Localization of p35 (annexin I, lipocortin I) in normal adult rat kidney and during recovery from ischemia

• Published in: Journal of cellular physiology Vol. 153; no. 3; p. 467
• Main Authors: McKanna, J A, Chuncharunee, A, Munger, K A, Breyer, J A, Cohen, S, Harris, R C
• Format: Journal Article
• Language: English
• Published: United States 01.12.1992
• Subjects: Animals; Annexin A1 - analysis; Epidermal Growth Factor - metabolism; Immunohistochemistry; Ischemia - metabolism; Kidney - blood supply; Kidney - metabolism; Kidney Tubular Necrosis, Acute - metabolism; Kidney Tubular Necrosis, Acute - pathology; Mitosis; Rats; Reference Values; Reperfusion; Tissue Distribution
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041530305

The 35-kDa protein (p35, lipocortin I, annexin I), originally discovered as a Ca(++)-dependent substrate for the EGF receptor tyrosine kinase, binds Ca++ and phospholipids, is developmentally regulated in embryos and has restricted expression in adults. Immunohistochemistry of normal rat kidney shows that p35 is enriched in epithelia of Bowman's capsule, the macula densa, and medullary/papillary collecting ducts, suggesting that p35 is related to specialized renal functions. Light staining is observed in the thick ascending limb; elsewhere, immunoreactivity is nil. Since renal recovery from ischemia involves both hyperplasia and hypertrophy and reportedly is accelerated by EGF, we examined p35 distribution during this process. After 48 hours of recovery, both the distribution and amount of renal p35 are altered. Immunoblots show p35 levels increased at least threefold in whole-kidney homogenates. The expression of p35 is still highly restricted in recovering kidneys; however, the thick ascending limb now stains heavily. This is the first documentation of alterations in annexin levels during a pathophysiologic response. However, our attempts to discern effects of exogenous EGF on the recovery from ischemia were negative for both mitotic index and renal function assays.