{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,24]],"date-time":"2025-07-24T12:25:11Z","timestamp":1753359911001},"reference-count":50,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2015,8,24]],"date-time":"2015-08-24T00:00:00Z","timestamp":1440374400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"National Council for Scientific and Technological Development of Brazil (CNPq)","award":["300122\/2010-1"],"award-info":[{"award-number":["300122\/2010-1"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:sec><jats:label \/><jats:p>The effects of kinin B<jats:sub>1<\/jats:sub> receptor (B<jats:sub>1<\/jats:sub>R) deletion were examined on femur bone regeneration in streptozotocin (STZ)\u2010type 1 diabetes. Diabetes induction in wild\u2010type C57\/BL6 (WTC57BL6) mice led to decrease in body weight and hyperglycemia, compared to the non\u2010diabetic group of the same strain. The lack of B<jats:sub>1<\/jats:sub>R did not affect STZ\u2010elicited body weight loss, but partially prevented hyperglycemia. Diabetic mice had a clear delay in bone regeneration, and displayed large areas of loose connective tissue within the defects, with a reduced expression of the mineralization\u2010related protein osteonectin, when compared to the non\u2010diabetic WTC57\/BL6. The non\u2010diabetic and diabetic B<jats:sub>1<\/jats:sub>R knockout (B<jats:sub>1<\/jats:sub>RKO) mice had bone regeneration levels and osteonectin expression comparable to that seen in control WTC57\/BL6 mice. WTC57\/BL6 STZ\u2010diabetic mice also showed a marked reduction of collagen contents, with increased immunolabeling for the apoptosis marker caspase\u20103, whereas diabetic B<jats:sub>1<\/jats:sub>RKO had collagen levels and caspase\u20103 activity comparable to those observed in non\u2010diabetic WTC57\/BL6 or B<jats:sub>1<\/jats:sub>RKO mice. No significant difference was detected in the number of tartrate\u2010resistant acid phosphatase (TRAP)\u2010stained cells, or in RANK\/RANKL\/OPG system immunolabeling throughout the experimental groups. Data bring novel evidence on the relevance of kinin B<jats:sub>1<\/jats:sub>R under type 1 diabetes with regards to its role in bone regeneration. J. Cell. 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