TRPM7 channels regulate proliferation and adipogenesis in 3T3-L1 preadipocytes

Chen, Kui-Hao; Xu, Xiaohui; Liu, Yi; Hu, Yan; Jin, Man-Wen; Li, Gui-Rong

doi:10.1002/jcp.24417

Cited by 17 publications

(15 citation statements)

References 41 publications

(61 reference statements)

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“…TRPV3 overexpression in the 3T3-L1 cells suppressed adipogenesis (8). The TRPV3 activators prevented high fat diet-induced enlargement of fat depots and weight gain (9). Visceral and subcutaneous adipose tissue from mice on chronic high fat diets, ob/ob and db/m ϩ mice expressed lower levels of TRPV3 than wild-type mice.…”

Section: Discussionmentioning

confidence: 99%

“…The heteromeric TRPC1/C5 channel negatively regulated adiponectin secretion in the adipocytes (8). TRPM7 facilitated adipocyte proliferation and differentiation in the 3T3-L1 preadipocytes (9). A previous report also demonstrated that the 3T3-L1 preadipocytes expressed higher levels of TRPV1, TRPV3, TRPM8, TRPC4 and TRPC6 than the differentiated adipocytes (10).…”

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confidence: 93%

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Activation of Transient Receptor Potential Vanilloid 3 Channel Suppresses Adipogenesis

et al. 2015

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The present study shows that activation of the transient receptor potential vanilloid 3 channel (TRPV3) suppresses adipocyte differentiation. We also found that a major functional catechin compound in green tea and cocoa, (-)-epicatechin, exerts antiadipogenic effects in the adipocytes through direct activation of TRPV3. TRPV3 was detected in the 3T3-L1 adipocytes using immunohistochemistry and semiquantitative PCR. TRPV3 activation by activators (-)-epicatechin and diphenylborinic anhydride was determined using live cell fluorescent Ca(2+) imaging and patch-clamp electrophysiology. Using RNA interference, immunoblotting, and Oil red O staining, we found that the TRPV3 agonists prevented adipogenesis by inhibiting the phosphorylation of insulin receptor substrate 1, the downstream phosphoinositide 3-kinase/Akt/forkhead box protein O1 axis, and the expression of the adipogenic genes peroxisome proliferator-activated receptor γ and CCAAT/enhancer-binding protein α. TRPV3 overexpression hindered adipogenesis in the 3T3-L1 cells. In vivo studies showed that chronic treatment with the TRPV3 activators prevented adipogenesis and weight gain in the mice fed on high-fat diets. Moreover, TRPV3 expression was reduced in the visceral adipose tissue from mice fed on high-fat diets and obese (ob/ob) and diabetic (db/m(+)) mice. In conclusion, our study illustrates the antiadipogenic role of TRPV3 in the adipocytes.

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Section: Discussionmentioning

confidence: 99%

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confidence: 93%

Activation of Transient Receptor Potential Vanilloid 3 Channel Suppresses Adipogenesis

et al. 2015

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“…In pre‐adipocytes, it has been reported that TRPM7 is functionally expressed and involved in proliferation and adipogenesis (Chen et al ). Consistently, we examined TRPM7 mRNA expression in 3T3‐L1 pre‐adipocytes and found that the expression levels of TRPM7 were comparable between pre‐adipocytes and differentiated 3T3‐L1 adipocytes (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Functional expression of TRPM7 as a Ca²⁺influx pathway in adipocytes

et al. 2019

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In adipocytes, intracellular Ca2+ and Mg2+ modulates physiological functions, such as insulin action and the secretion of adipokines. TRPM7 is a Ca2+/Mg2+‐permeable non‐selective cation channel. TRPM7 mRNA is highly expressed in adipose tissue, however, its functional expression in adipocytes remains to be elucidated. In this study, we demonstrated for the first time that TRPM7 was functionally expressed in both freshly isolated white adipocytes and in 3T3‐L1 adipocytes differentiated from a 3T3‐L1 pre‐adipocyte cell line by whole‐cell patch‐clamp recordings. Consistent with known properties of TRPM7 current, the current in adipocytes was activated by the elimination of extracellular divalent cations and the reduction of intracellular free Mg2+ concentrations, and was inhibited by the TRPM7 inhibitors, 2‐aminoethyl diphenylborinate (2‐APB), hydrogen peroxide (H2O2), N‐methyl maleimide (NMM), NS8593, and 2‐amino‐2‐[2‐(4‐octylphenyl)ethyl]‐1,3‐propanediol (FTY720). Treatment with small‐interfering (si) RNA targeting TRPM7 resulted in a reduction in the current to 23 ± 7% of nontargeting siRNA‐treated adipocytes. Moreover a TRPM7 activator, naltriben, increased the TRPM7‐like current and [Ca2+]i in 3T3‐L1 adipocytes but not in TRPM7‐knockdown adipocytes. These findings indicate that TRPM7 is functionally expressed, and plays a role as a Ca2+ influx pathway in adipocytes.

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“…Cell proliferation was determined using 3-(4, 5-dimethyl-thiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) and 5-bromo-2’-deoxyuridine (BrdU) incorporation assay as described previously [40, 41]. For MTT assays, cells were plated into 96-well plates at a density of ~3000 cells/well in 200 μL normal culture medium for 12 h. Different concentrations of bradykinin with or without HOE140 in α-MEM with 1% FBS were added into each well.…”

Section: Meterials and Methodsmentioning

confidence: 99%

Bradykinin regulates cell growth and migration in cultured human cardiac c-Kit+ progenitor cells

2017

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Bradykinin is a well-known endogenous vasoactive peptide. The present study investigated the bradykinin receptor expression in human cardiac c-Kit+ progenitor cells and the potential role of bradykinin in regulating cell cycling progression and mobility. It was found that mRNA and protein of bradykinin type 2 receptors, but not bradykinin type 1 receptors, were abundant in cultured human cardiac c-Kit+ progenitor cells. Bradykinin (1-10 nM) stimulated cell growth and migration in a concentration-dependent manner. The increase of cell proliferation was related to promoting G0/G1 transition into G2/M and S phase. Western blots revealed that bradykinin significantly increased pAkt and pERK1/2 as well as cyclin D1, which were countered by HOE140 (an antagonist of bradykinin type 2 receptors) or by silencing bradykinin type 2 receptors. The increase of pAkt, pERK1/2 and cyclin D1 by bradykinin was prevented by the PI3K inhibitor Ly294002, the PLC inhibitors U73122 and neomycin, and/or the PKC inhibitor chelerythrine and the MAPK inhibitor PD98059. Our results demonstrate the novel information that bradykinin promotes cell cycling progression and migration in human cardiac c-Kit+ progenitor cells via activating PI3K, PLC, PKC, cyclin D1, pERK1/2, and pAkt.

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TRPM7 channels regulate proliferation and adipogenesis in 3T3-L1 preadipocytes

Cited by 17 publications

References 41 publications

Activation of Transient Receptor Potential Vanilloid 3 Channel Suppresses Adipogenesis

Activation of Transient Receptor Potential Vanilloid 3 Channel Suppresses Adipogenesis

Functional expression of TRPM7 as a Ca²⁺influx pathway in adipocytes

Bradykinin regulates cell growth and migration in cultured human cardiac c-Kit+ progenitor cells

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TRPM7 channels regulate proliferation and adipogenesis in 3T3-L1 preadipocytes

Cited by 17 publications

References 41 publications

Activation of Transient Receptor Potential Vanilloid 3 Channel Suppresses Adipogenesis

Activation of Transient Receptor Potential Vanilloid 3 Channel Suppresses Adipogenesis

Functional expression of TRPM7 as a Ca2+influx pathway in adipocytes

Bradykinin regulates cell growth and migration in cultured human cardiac c-Kit+ progenitor cells

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Functional expression of TRPM7 as a Ca²⁺influx pathway in adipocytes