Department of Neurological Surgery, UCSF, San Francisco, CA 94158, USA; SFVAMC, San Francisco, CA 94121, USA; Department of Neurosurgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan.
Department of Neurological Surgery, UCSF, San Francisco, CA 94158, USA; SFVAMC, San Francisco, CA 94121, USA; Linköping University, Linköping SE-581 83, Sweden.
Exp Neurol. 2020 Dec;334:113461. doi: 10.1016/j.expneurol.2020.113461. Epub 2020 Sep 12.
We investigated whether type 2 diabetes mellitus (T2DM), a risk factor of stroke, affects the level of scavenger receptor CD36 and the uptake of its ligand, oxidized LDL (oxLDL); and whether pioglitazone, a drug that enhances CD36, promotes oxLDL uptake. Compared to normoglycemic db/+ mice, adult db/db mice showed a pronounced reduction in surface CD36 expression on myeloid cells from the blood, brain, and bone marrow as detected by flow cytometry, which correlated with elevated plasma soluble-CD36 as determined by ELISA. Increased CD36 expression was found in brain macrophages and microglia of both genotypes 7 days after ischemic stroke. In juvenile db/db mice, prior to obesity and hyperglycemia, only a mild reduction of surface CD36 was found in blood neutrophils, while all other myeloid cells showed no difference relative to the db/+ strain. In vivo, oral pioglitazone treatment for four weeks increased CD36 levels on myeloid cells in db/db mice. In vitro, uptake of oxLDL by bone marrow derived macrophages (BMDMs) of db/db mice was reduced relative to db/+ mice in normal glucose medium. OxLDL uptake inversely correlated with glucose levels in the medium in db/+ BMDMs. Furthermore, pioglitazone restored oxLDL uptake by BMDMs from db/db mice cultured in high glucose. Our data suggest that T2DM is associated with reduced CD36 on adult myeloid cells, and pioglitazone enhances CD36 expression in db/db cells. T2DM or high glucose reduces oxLDL uptake while pioglitazone enhances oxLDL uptake. Our findings provide new insight into the mechanism by which pioglitazone may be beneficial in the treatment of insulin resistance.
我们研究了 2 型糖尿病(T2DM)这一卒中危险因素是否会影响清道夫受体 CD36 的水平及其配体氧化型 LDL(oxLDL)的摄取;以及是否吡格列酮(一种增强 CD36 的药物)可促进 oxLDL 的摄取。与血糖正常的 db/+ 小鼠相比,流式细胞术检测发现成年 db/db 小鼠血液、大脑和骨髓中的髓样细胞表面 CD36 表达明显减少,这与 ELISA 检测到的血浆可溶性 CD36 升高相关。两种基因型缺血性卒中 7 天后,均发现大脑巨噬细胞和小胶质细胞 CD36 表达增加。在幼年 db/db 小鼠中,在肥胖和高血糖之前,仅发现血液中性粒细胞表面 CD36 轻度减少,而所有其他髓样细胞与 db/+ 品系相比均无差异。体内,口服吡格列酮治疗 4 周可增加 db/db 小鼠髓样细胞的 CD36 水平。体外,在正常葡萄糖培养基中,db/db 小鼠骨髓来源的巨噬细胞(BMDM)摄取 oxLDL 的能力相对于 db/+ 小鼠降低。oxLDL 摄取与 db/+ BMDM 培养基中的葡萄糖水平呈负相关。此外,吡格列酮可恢复高糖培养的 db/db 小鼠 BMDM 摄取 oxLDL。我们的数据表明,T2DM 与成年髓样细胞上 CD36 减少有关,吡格列酮可增强 db/db 细胞的 CD36 表达。T2DM 或高血糖可降低 oxLDL 的摄取,而吡格列酮可增强 oxLDL 的摄取。我们的研究结果为吡格列酮在治疗胰岛素抵抗中的作用机制提供了新的见解。