Kinin B sub(1) Receptor Deletion Affects Bone Healing in Type 1 Diabetic Mice

• Published in: Journal of cellular physiology 2015-12, Vol.230 (12), p.3019-3028
• Main Authors: Cignachi, Natalia P, Pesquero, Joao B, Oliveira, Rogerio B, Etges, Adriana, Campos, Maria M
• Format: Article
• Language: English
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.25034

The effects of kinin B sub(1) receptor (B sub(1)R) 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 B sub(1)R 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 B sub(1)R knockout (B sub(1)RKO) 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 B sub(1)RKO had collagen levels and caspase-3 activity comparable to those observed in non-diabetic WTC57/BL6 or B sub(1)RKO 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 B sub(1)R under type 1 diabetes with regards to its role in bone regeneration. J. Cell. Physiol. 230: 3019-3028, 2015.