Background/Aims: α<sub>8</sub>β<sub>1</sub>-Integrin is expressed in mesangial cells. In vitro studies suggest a role for α<sub>8</sub>-integrin in the regulation of cell proliferation and apoptosis. We tested the hypothesis that α<sub>8</sub>-integrin is essential for the healing process after mesangioproliferative glomerulonephritis. Methods: Mice homozygous for a deletion of the α<sub>8</sub>-integrin chain were compared with wild-type mice. To study glomerular healing, we used the habu toxin model of reversible mesangioproliferative glomerulonephritis. Animals received 6 mg/kg habu toxin intravenously; controls received saline only. Results: Early mesangiolysis occurred in wild-type and α<sub>8</sub>-integrin-deficient mice. However, mesangiolysis was no longer detectable after 7 days in wild types but persisted after 14 days in α<sub>8</sub>-integrin-deficient animals. Mesangial activation marker α-smooth muscle actin was detectable only at day 7 in wild-type mice but persisted until day 14 in α<sub>8</sub>-integrin-deficient mice. In wild types, glomerular cell proliferation and apoptosis peaked at day 7 and decreased thereafter but remained elevated in α<sub>8</sub>-integrin-deficient mice until day 28. In cultivated mesangial cells, α<sub>8</sub>-integrin expression was associated with increased cell survival. Conclusion: Interactions between α<sub>8</sub>-integrin and the mesangial matrix may contribute to healing of glomerular injury by influencing cell proliferation and apoptosis.