title: Kinin B1 Receptor Deletion Affects Bone Healing in Type 1 Diabetic Mice.
abstract: The effects of kinin B1 receptor (B1 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 B1 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 B1 R knockout (B1 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 B1 RKO had collagen levels and caspase-3 activity comparable to those observed in non-diabetic WTC57/BL6 or B1 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 B1 R under type 1 diabetes with regards to its role in bone regeneration.
authors.affiliation: School of Dentistry, Pontifical Catholic University of Rio Grande do Sul, Avenida Ipiranga, 6681, Partenon, Porto Alegre, RS, Brazil.
authors.forename: Natália P
authors.initials: NP
authors.lastname: Cignachi
authors.affiliation: Department of Biophysics, Federal University of São Paulo, Rua Pedro de Toledo, 669, São Paulo, SP, Brazil.
authors.forename: João B
authors.initials: JB
authors.lastname: Pesquero
authors.affiliation: School of Dentistry, Pontifical Catholic University of Rio Grande do Sul, Avenida Ipiranga, 6681, Partenon, Porto Alegre, RS, Brazil.
authors.forename: Rogério B
authors.initials: RB
authors.lastname: Oliveira
authors.affiliation: Department of Oral Pathology, School of Dentistry, Universidade Federal de Pelotas (UFPel), Rua, Gonçalves Chaves, 457, Pelotas, RS, Brazil.
authors.forename: Adriana
authors.initials: A
authors.lastname: Etges
authors.affiliation: School of Dentistry, Pontifical Catholic University of Rio Grande do Sul, Avenida Ipiranga, 6681, Partenon, Porto Alegre, RS, Brazil.|Institute of Toxicology and Pharmacology, Pontifical Catholic University of Rio Grande do Sul, Avenida Ipiranga, 6681, Partenon, Porto Alegre, RS, Brazil.
authors.forename: Maria M
authors.initials: MM
authors.lastname: Campos
mesh_terms: D000818:Animals; D017209:Apoptosis; D001861:Bone Regeneration; D053148:Caspase 3 / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D005264:Femoral Fractures / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D005269:Femur / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D017102:Fracture Healing; D008297:Male; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D015676:Osteonectin / Q000378:metabolism; D043783:Receptor, Bradykinin B1 / Q000172:deficiency* / Q000235:genetics; D015398:Signal Transduction; D013997:Time Factors
chemical_list: D015676:Osteonectin; D043783:Receptor, Bradykinin B1; D003094:Collagen; C505409:Casp3 protein, mouse; D053148:Caspase 3