Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury

Kamyar Zahedi, Monica P. Revelo, Sharon Barone, Zhaohui Wang, Kathy Tehrani, David P. Citron, John Bissler, Hamid Rabb, Manoocher Soleimani

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

In kidneys subjected to ischemic reperfusion injury (IRI) stathmin, a tubulin-binding protein involved in the regulation of mitosis, is expressed in dedifferentiated and proliferating renal tubule cells during the recovery phase. To ascertain the role of stathmin in the recovery from ischemic kidney injury, stathmin-deficient (OP18-/-) and wild-type (WT) animals were subjected to experimental IRI. At 3, 7, and 14 days after reperfusion serum samples and kidneys were collected for the examination of parameters of renal function, morphology, and recovery. Our studies indicate that on day 14 after reperfusion OP18-/- mice have significant renal failure, whereas the creatinine levels of WT animals have returned to baseline. Compared with WT animals OP18-/- mice had more extensive tubular fibrosis. The examination of proliferating cell nuclear antigen expression indicated that OP18-/- animals have increased proliferative or DNA repair activity for a more prolonged duration. The OP18-/- animals also had an increased number of tubules with apoptotic cells. These results suggest that in stathmin-deficient mice subjected to IRI, the aberrant regulation of cell cycle progression, not observed under normal conditions, impairs or at least delays the process of tubular repair and recovery after acute renal injury.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Physiology
Volume290
Issue number6
DOIs
StatePublished - Jun 1 2006

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Stathmin
Reperfusion Injury
Fibrosis
Wild Animals
Kidney
Reperfusion
Recovery of Function
Proliferating Cell Nuclear Antigen
Tubulin
Acute Kidney Injury
Mitosis
DNA Repair
Renal Insufficiency
Creatinine
Cell Cycle
Carrier Proteins
Wounds and Injuries
Serum

All Science Journal Classification (ASJC) codes

  • Physiology
  • Urology

Cite this

Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury. / Zahedi, Kamyar; Revelo, Monica P.; Barone, Sharon; Wang, Zhaohui; Tehrani, Kathy; Citron, David P.; Bissler, John; Rabb, Hamid; Soleimani, Manoocher.

In: American Journal of Physiology - Renal Physiology, Vol. 290, No. 6, 01.06.2006.

Research output: Contribution to journalArticle

Zahedi, Kamyar ; Revelo, Monica P. ; Barone, Sharon ; Wang, Zhaohui ; Tehrani, Kathy ; Citron, David P. ; Bissler, John ; Rabb, Hamid ; Soleimani, Manoocher. / Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury. In: American Journal of Physiology - Renal Physiology. 2006 ; Vol. 290, No. 6.
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