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

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.

Induction of Zf9 in the kidney following early ischemia/reperfusion.

Background: An improved understanding of the early cell injury mechanisms is critical for effective therapy of acute renal failure (ARF).

Methods: We utilized cDNA microarrays to identify renal genes that are induced very early after renal ischemia in a mouse model, whose protein products might provide novel information regarding the pathogenesis of ARF. The findings were confirmed by downstream mRNA and protein expression studies, as well as knockdown analysis with antisense primers.

Overexpression of SSAT in kidney cells recapitulates various phenotypic aspects of kidney ischemia-reperfusion injury.

To ascertain the role of spermidine/spermine N-1-acetyl-transferase (SSAT; the rate-limiting enzyme in polyamine catabolism) in cell injury, cultured kidney (HEK 293) cells conditionally overexpressing SSAT were generated. The SSAT expression was induced and its enzymatic activity increased 24 h after addition of tetracycline and remained elevated over the length of the experiments. Induction of SSAT upregulated the expression of polyamine oxidase and resulted in the reduction of cellular concentration of spermidine and spermine, increased concentration of putrescine, and inhibited cell growth.

Identification of stathmin as a novel marker of cell proliferation in the recovery phase of acute ischemic renal failure.

Ischemic renal injury can be classified into the initiation and extension phase followed by the recovery phase. The recovery phase is characterized by increased dedifferentiated and mitotic cells in the damaged tubules. Suppression subtractive hybridization was performed by using RNA from normal and ischemic kidneys to identify the genes involved in the physiological response to ischemia-reperfusion injury (IRI).