CD36 is involved in high glucose-induced epithelial to mesenchymal transition in renal tubular epithelial cells.
The epithelial-to-mesenchymal transition (EMT) plays an important role in the progression of diabetic nephropathy. Our recent study showed that ROS mediated high glucose (HG)-induced EMT in renal tubular epithelial cells. CD36, a class-B scavenger receptor, has been reported to mediate the production of ROS in chronic kidney disease. In the present study, we examined the effect of inhibition of CD36 with CD36 siRNA or sulfosuccinimidyl-oleate (SSO), a CD36 antagonist, on HG-induced EMT in HK-2 cells. HG induced CD36 expression in a time-dependent manner in HK-2 cells. HG was shown to induce EMT at 72 h. This was blocked by knockdown of CD36 or treatment with SSO. Meanwhile, we also found that knockdown of CD36 or treatment with SSO inhibited HG-induced ROS generation, activation of ERK1/2 and Smad2, expression of TGF-β1 and synthesis of fibronectin. These data suggest that inhibition of CD36 prevented HG-induced EMT in HK-2 cells, highlighting CD36 as a potential therapeutic target for diabetic nephropathy.
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang 050017, China; Department of Nephrology, Third Hospital, Hebei Medical University, Shijiazhuang 050051, China; Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
Yanjuan
Y
Hou
Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
Ming
M
Wu
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang 050017, China; Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
Jinying
J
Wei
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang 050017, China; Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
Yunzhuo
Y
Ren
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang 050017, China; Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
Chunyang
C
Du
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang 050017, China; Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
Haijiang
H
Wu
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang 050017, China; Department of Nephrology, Third Hospital, Hebei Medical University, Shijiazhuang 050051, China. Electronic address: hebeiliying@126.com.
Ying
Y
Li
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang 050017, China; Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China. Electronic address: yonghongshi@126.com.
Yonghong
Y
Shi
D018955:CD36 Antigens / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002460:Cell Line; D003928:Diabetic Nephropathies / Q000378:metabolism*; D004847:Epithelial Cells / Q000166:cytology* / Q000378:metabolism; D058750:Epithelial-Mesenchymal Transition; D005353:Fibronectins / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007684:Kidney Tubules / Q000166:cytology* / Q000378:metabolism; D020935:MAP Kinase Signaling System; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D051785:Smad Proteins / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
D018955:CD36 Antigens; D005353:Fibronectins; D017382:Reactive Oxygen Species; D051785:Smad Proteins; D053773:Transforming Growth Factor beta1; D005947:Glucose
CD36; Epithelial to mesenchymal transition; High glucose; Oxidative stress; Renal tubular epithelial cell