Down-regulation of integrin β1 and focal adhesion kinase in renal glomeruli under various hemodynamic conditions.
Given that integrin β1 is an important component of the connection to maintain glomerular structural integrity, by binding with multiple extracellular matrix proteins and mediating intracellular signaling. Focal adhesion kinase (FAK) is the most essential intracellular integrator in the integrin β1-FAK signalling pathway. Here, we investigated the changes of the two molecules and visualized the possible interaction between them under various hemodynamic conditions in podocytes. Mice kidney tissues were prepared using in vivo cryotechnique (IVCT) and then were stained and observed using light microscopy, confocal laser scanning microscopy and immunoelectron microscopy. The expression of these molecules were examined by western blot. Under the normal condition, integrin β1 stained continually and evenly at the membrane, and FAK was located in the cytoplasm and nuclei of the podocytes. There were significant colocalized plaques of two molecules. But under acute hypertensive and cardiac arrest conditions, integrin β1 decreased and stained intermittently. Similarly, FAK decreased and appeared uneven. Additionally, FAK translocated to the nuclei of the podocytes. As a result, the colocalization of integrin β1 and FAK reduced obviously under these conditions. Western blot assay showed a consistent result with the immunostaining. Collectively, the abnormal redistribution and decreased expressions of integrin β1 and FAK are important molecular events in regulating the functions of podocytes under abnormal hemodynamic conditions. IVCT could offer considerable advantages for morphological analysis when researching renal diseases.
Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, China; Department of Nephrology, General Hospital of Tisco, Shanxi Medical University, Taiyuan, China.
Xiaoli
X
Yuan
Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, China.
Wei
W
Wang
Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, China.
Juan
J
Wang
Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, China.
Xiaohui
X
Yin
Department of Histology and Embryology, Institute of Pathology and Pathophysiology, China Medical University, Shenyang, China.
Xiaoyue
X
Zhai
Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, China.
Lining
L
Wang
Department of Surgical Oncology, First Affiliated Hospital of China Medical University, Shenyang, China.
Kai
K
Li
Department of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, China.
Zilong
Z
Li
D000818:Animals; D015536:Down-Regulation; D005455:Fluorescent Antibody Technique; D051416:Focal Adhesion Protein-Tyrosine Kinases / Q000378:metabolism*; D006439:Hemodynamics; D006973:Hypertension / Q000378:metabolism; D007150:Immunohistochemistry; D019012:Integrin beta1 / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000473:pathology / Q000502:physiology* / Q000503:physiopathology / Q000648:ultrastructure; D051379:Mice; D050199:Podocytes / Q000378:metabolism; D021381:Protein Transport
D019012:Integrin beta1; D051416:Focal Adhesion Protein-Tyrosine Kinases