Expression of Connexins 43, 26 and 32 in normal, hyperplastic and neoplastic perianal dog glands

Connexin (Cx) expression is reportedly altered in neoplasms. This study aimed to investigate the expression of Cx43, 26 and 32 in normal and pathological canine perianal glands. Thirty perianal glands bearing pathological processes and ten normal canine perianal glands were submitted to immunohistochemistry to search for presence of Cx43, Cx26 and Cx32. Both Cx43 and Cx26 expressions were observed in normal, hyperplastic glands, and in well and moderately differentiated adenomas. However, in poorly differentiated adenomas, expressions were reduced, and they were absent in carcinomas. Cx26 was located in the cytoplasm of normal, hyperplastic perianal gland cells, and in well and moderately differentiated adenomas. Cx32 was not observed in any neoplasm neither in normal or hyperplastic glands. Our results show that Cx43 and Cx26 expressions are altered in more aggressive canine perianal gland neoplasms, and we conclude that they may be related to the perianal gland carcinogenesis process

Diminished angiogenesis in the cornea of mice with heterologous deletion of Connexin 43 gene (Gja1)

Angiogenesis is involved in several physiological and pathological processes, and the proliferation of endothelial cells is a central event in the generation of new blood vessels. Gap junctions (GJ) are membrane structures that communicate adjacent cells, contribute to tissue homeostasis, and are important to the control of cell proliferation. Connexins (Cxs) are the proteins that form gap junctions. Endothelial cells may express Cx43, Cx37 and Cx40. In this study, we analyzed the effect of the heterologous deletion of the Gja1 (Cx43 gene) on the development of newly formed blood vessels (NFBV) in the mouse cornea. Heterozygous (Cx43+/-) and wild-type (Cx43+/+) mice were submitted to the silver crystal corneal cauterization model. Two parameters were quantified by image analysis 2 or 6 days after cauterization: NFBV density and length. At days 2 and 6 after corneal cauterization, Cx43+/- mice showed smaller density of NFBV as compared to Cx43+/+ mice. Therefore, deletion of one Gja1 allele (connexin-43 gene) may lead to impaired cell-cell communication in endothelial cells, diminishing angiogenesis after cauterization of the mouse cornea

Diminished angiogenesis in the cornea of mice with heterologous deletion of Connexin 43 gene (Gja1)

Angiogenesis is involved in several physiological and pathological processes, and the proliferation of endothelial cells is a central event in the generation of new blood vessels. Gap junctions (GJ) are membrane structures that communicate adjacent cells, contribute to tissue homeostasis, and are important to the control of cell proliferation. Connexins (Cxs) are the proteins that form gap junctions. Endothelial cells may express Cx43, Cx37 and Cx40. In this study, we analyzed the effect of the heterologous deletion of the Gja1 (Cx43 gene) on the development of newly formed blood vessels (NFBV) in the mouse cornea. Heterozygous (Cx43+/-) and wild-type (Cx43+/+) mice were submitted to the silver crystal corneal cauterization model. Two parameters were quantified by image analysis 2 or 6 days after cauterization: NFBV density and length. At days 2 and 6 after corneal cauterization, Cx43+/- mice showed smaller density of NFBV as compared to Cx43+/+ mice. Therefore, deletion of one Gja1 allele (connexin-43 gene) may lead to impaired cell-cell communication in endothelial cells, diminishing angiogenesis after cauterization of the mouse cornea(AU)

Expression of Connexins 43, 26 and 32 in normal, hyperplastic and neoplastic perianal dog glands

Connexin (Cx) expression is reportedly altered in neoplasms. This study aimed to investigate the expression of Cx43, 26 and 32 in normal and pathological canine perianal glands. Thirty perianal glands bearing pathological processes and ten normal canine perianal glands were submitted to immunohistochemistry to search for presence of Cx43, Cx26 and Cx32. Both Cx43 and Cx26 expressions were observed in normal, hyperplastic glands, and in well and moderately differentiated adenomas. However, in poorly differentiated adenomas, expressions were reduced, and they were absent in carcinomas. Cx26 was located in the cytoplasm of normal, hyperplastic perianal gland cells, and in well and moderately differentiated adenomas. Cx32 was not observed in any neoplasm neither in normal or hyperplastic glands. Our results show that Cx43 and Cx26 expressions are altered in more aggressive canine perianal gland neoplasms, and we conclude that they may be related to the perianal gland carcinogenesis process (AU)