Depletion of Kindlin-2 induces cardiac dysfunction in mice

Autor: Lihua Qi, Yao Song, Youyi Zhang, Xiaochun Chi, Hongquan Zhang, Danyu Lu, Yu Yu
Rok vydání: 2016
Předmět:
0301 basic medicine
Cardiac function curve
Male
medicine.medical_specialty
Time Factors
Blotting
Western
Muscle Proteins
Blood Pressure
030204 cardiovascular system & hematology
General Biochemistry
Genetics and Molecular Biology
Cardiac dysfunction
Muscle hypertrophy
Focal adhesion
03 medical and health sciences
0302 clinical medicine
Environmental Science(all)
Internal medicine
medicine
Animals
Cardiac structure
Myocytes
Cardiac
General Environmental Science
Mice
Inbred ICR
Microscopy
Confocal
Agricultural and Biological Sciences(all)
business.industry
Biochemistry
Genetics and Molecular Biology(all)
Myocardium
Cardiac myocyte
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Heart
Anatomy
Organ Size
medicine.disease
Cytoskeletal Proteins
030104 developmental biology
Endocrinology
Echocardiography
cardiovascular system
RNA Interference
General Agricultural and Biological Sciences
business
Zdroj: Science China. Life sciences. 59(11)
ISSN: 1869-1889
Popis: Kindlin-2, a member of the Kindlin family focal adhesion proteins, plays an important role in cardiac development. It is known that defects in the Z-disc proteins lead to hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM). Our previous investigation showed that Kindlin-2 is mainly localized at the Z-disc and depletion of Kindlin-2 disrupts the structure of the Z-Disc. Here, we reported that depletion of Kindlin-2 leads to the disordered myocardial fibers, fractured and vacuolar degeneration in myocardial fibers. Interestingly, depletion of Kindlin-2 in mice induced cardiac myocyte hypertrophy and increased the heart weight. Furthermore, decreased expression of Kindlin-2 led to cardiac dysfunction and also markedly impairs systolic function. Our data indicated that Kindlin-2 not only maintains the cardiac structure but also is required for cardiac function.
Databáze: OpenAIRE
Externí odkaz: