MIP-1α Induction by Palmitate in the Human Monocytic Cells Implicates TLR4 Signaling Mechanism

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
Rasheed AhmadSardar Sindhu

Abstract

MIP-1α (macrophage inflammatory protein 1α)/CCL3 chemokine is associated with the adipose tissue inflammation in obesity. Both MIP-1α and free fatty acids are elevated in obesity/T2D. We asked if free fatty acid palmitate could modulate MIP1α expression in the human monocytic cells. Human monocytic THP-1 cells and macrophages were stimulated with palmitate and TNF-α (positive control). MIP-1α expression was measured with real time RT-PCR, Flow Cytometry and ELISA. Signaling pathways were identified by using THP-1-XBlue™ cells, THP-1-XBlue™-defMyD cells, anti-TLR4 mAb and TLR4 siRNA. Our data show that palmitate induced significant increase in MIP1α production in monocytic THP-1 cells/macrophages. MIP-1α induction was significantly suppressed when cells were treated with anti-TLR4 antibody prior stimulation with palmitate. Using TLR4 siRNA, we further demonstrate that palmitate-induced MIP-1α expression in monocytic cells requires TLR4. Moreover, THP1 cells defective in MyD88, a major adaptor protein involved in TLR4 signaling, were unable to induce MIP-1α production in response to palmitate. Palmitate-induced MIP-1α expression was suppressed by inhibition of MAPK, NFkB and PI3K signaling pathways. In addition, palmitate-induced...Continue Reading

Citations

Sep 10, 2019·Frontiers in Immunology·Omar SharifGernot Schabbauer
Jul 25, 2021·International Journal of Molecular Sciences·Areej Al-RoubRasheed Ahmad
Sep 17, 2021·Molecular and Cellular Biochemistry·Rahul Mallick, Asim K Duttaroy

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