http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Subramani Manigandan (검색결과 4 건)
- 무료
- 기관 내 무료
- 유료
-
Manigandan SUBRAMANI,Jong Won YUN 한국생물공학회 2021 한국생물공학회 학술대회 Vol.2021 No.10
Lymphocyte cytosolic protein 1 (LCP1) plays a vital role in non-hematopoietic malignancies, and is also a well-known tumor biomarker; however, evidence regarding its function in adipocytes remains to be elucidated. The current study explores the physiological role of LCP1 in cultured 3T3-L1 white adipocytes, by applying the loss-of-function study using siRNA. Induction of fat browning by LCP1 depletion was evidenced by evaluating the gene and protein expression levels of brown fat-associated markers through real-time qRT-PCR and immunoblot analysis, respectively. We observed that deficiency of LCP1 promotes mitochondrial biogenesis, and significantly enhances expressions of the core brown fat-specific genes (Cd137, Cidea, Cited1, Tbx1, and Tmem26) and proteins (PGC-1α, PRDM16, and UCP1). In addition, deficiency of LCP1 promotes lipid catabolism as well as suppresses adipogenesis and lipogenesis. Loss of LCP1 also ameliorates cellular stress by downregulating JNK and c-JUN in adipocytes, and stimulates apoptosis. A mechanistic study revealed that deficiency of LCP1 induces browning in white adipocytes, independently via β3-AR and the ERK signaling pathway. The current data reveals a previously unknown mechanism of LCP1 in browning of white adipocytes, and highlights the potential of LCP1 as a pharmacotherapeutic target for treating obesity and other metabolic disorders.
-
-
Subramani Manigandan,윤종원 한국생물공학회 2020 Biotechnology and Bioprocess Engineering Vol.25 No.3
Recently, pharmacological activation of thermogenesis in brown fat and induction of white fat browning (beiging) have been considered as promising strategies in the development of anti-obesity drugs. During the screening of natural compounds that may stimulate thermogenesis, urolithin A (UroA), which is metabolized from pomegranate ellagitannins by gut microflora, was identified as a potent anti-obesity candidate. In the present study, we elucidated the role of UroA to induce the brown-like phenotype in 3T3-L1 white adipocytes. UroA treatments of up to 50 μM were non-toxic to cells. UroA at 15 μM significantly increased the protein expression levels of brown-fatspecific markers such as UCP1, PRDM16, PGC-1α, C/ EBPβ, and PPARα. In addition, it remarkably increased the expression of beige-specific genes, including Cd137, Cidea, Cited1, Tbx1, and Tmen26, in 3T3-L1 white adipocytes and significantly elevated expressions of the brown-fatspecific genes (Ppargc1, Prdm16, and Ucp1) in white adipocytes. Furthermore, UroA treatment of 3T3-L1 white adipocytes cells reduced the expression of key adipogenic transcription factors, whereas enhanced lipolysis and the fat oxidation process. Mechanistic study revealed that UroA treatment induces browning in white adipocytes via activation of β3-AR- and p38 MAPK-dependent signaling pathways. Taken together, UroA has the potential to treat obesity by its capacity to recruit beige fat cells in white adipocyte tissue, thereby contributing to an increase in thermogenesis.
-
SUBRAMANI MANIGANDAN,윤종원 한국생물공학회 2023 Biotechnology and Bioprocess Engineering Vol.28 No.4
Increasing the number of brite cells (browning) in white adipocytes has attracted considerable attention to combat obesity because brite cells also help elevate energy expenditure. Sodium-potassium adenosine triphosphatase α2 subunit (ATP1A2) has been studied extensively in migraine and cancers. On the other hand, the role of ATP1A2 in adipocytes biology with a focus on fat browning needs to be elucidated. In this study, suppression of ATP1A2 induced browning in white adipocytes. The siRNA-mediated knockdown was used to identify the functional roles of the ATP1A2 gene in white adipocytes browning and the lipid metabolism. A deficiency of ATP1A2 promoted the expression of brown adipocyte-specific proteins and genes, suppressed adipogenesis and lipogenesis, and enhanced lipolysis and fat oxidation, as well as mitochondrial biogenesis. Moreover, silencing of ATP1A2 enhanced the expression of marker proteins for UCP1-dependent (β3- AR, PKA, p38, ATF2, and ERK) and UCP1-independent (α1-AR, SERCA, and RyR) thermogenesis. A mechanistic study showed that a deficiency of ATP1A2 induces browning in white adipocytes by activating the β3-AR/ERK signaling pathways as well as α1-AR/SERCA-based thermogenesis through an ATP-consuming process. In conclusion, ATP1A2 is a previously unrecognized player in thermogenesis in white adipocytes, and downregulating ATP1A2 and activating both UCP1-dependent and UCP1-independent thermogenesis in adipocytes could be a novel pharmacotherapeutic approach to treat obesity.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
