Kinin B1 Receptor Deletion Affects Bone Healing in Type 1 Diabetic Mice.

Autor: Cignachi, Natália P., Pesquero, João B., Oliveira, Rogério B., Etges, Adriana, Campos, Maria M.
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Zdroj: Journal of Cellular Physiology; Dec2015, Vol. 230 Issue 12, p3019-3028, 10p
Abstrakt: The effects of kinin B1 receptor (B1R) deletion were examined on femur bone regeneration in streptozotocin (STZ)-type 1 diabetes. Diabetes induction in wild-type C57/BL6 (WTC57BL6) mice led to decrease in body weight and hyperglycemia, compared to the non-diabetic group of the same strain. The lack of B1R did not affect STZ-elicited 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-related protein osteonectin, when compared to the non-diabetic WTC57/BL6. The non-diabetic and diabetic B1R knockout (B1RKO) mice had bone regeneration levels and osteonectin expression comparable to that seen in control WTC57/BL6 mice. WTC57/BL6 STZ-diabetic mice also showed a marked reduction of collagen contents, with increased immunolabeling for the apoptosis marker caspase-3, whereas diabetic B1RKO had collagen levels and caspase-3 activity comparable to those observed in non-diabetic WTC57/BL6 or B1RKO mice. No significant difference was detected in the number of tartrate-resistant acid phosphatase (TRAP)-stained cells, or in RANK/RANKL/OPG system immunolabeling throughout the experimental groups. Data bring novel evidence on the relevance of kinin B1R under type 1 diabetes with regards to its role in bone regeneration. J. Cell. Physiol. 230: 3019-3028, 2015. © 2015 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index