Welcome to Wei Lab!
Wei lab belongs to Department of Immunology, School of Basic Medical Sciences, Fudan University. We study vascular immunology by focusing on non-coding RNAs and organelle interactions and attempt to get better understanding of  macrophage phenotypic plasticity and pathophysiology of atherosclerosis.

Regulation of microRNA (miRNA) function by modulating its biogenesis and targeting in the immune system. Immune cells orchestrate miRNA function through regulating or modifying the key enzymes and proteins involved in miRNA biogenesis, such as Exportin 5, Dicer, Ago2, and some RNA binding proteins (RBPs). Moreover, miRNAs may selectively target mRNAs according to the miRNA site types in distinct immune cells. miRNA-mediated targeting may also be regulated by competing endogenous RNA (ceRNAs) or affected by alternative poly(A) site usage in immune responses. The events in the miRNA biogenesis and targeting pathways that are able to be regulated during immune responses are summarized in the boxes outlined with dash lines and numbered according to the text. The arrows with solid lines indicate each step in the process of miRNA biogenesis, while the arrows with dash lines indicate how that step is modulated in immune cells.
Long non-coding RNAs (lncRNAs) represent crucial transcriptional and post-transcriptional gene regulators during antimicrobial responses in the host innate immune system. Studies have shown that lncRNAs are expressed in a highly tissue- and cell-specific- manner and are involved in the differentiation and function of innate immune cells, as well as inflammatory and antiviral processes, through versatile molecular mechanisms. These lncRNAs function via the interactions with DNA, RNA, or protein in either cis or trans pattern, relying on their specific sequences or their transcriptions and processing. The dysregulation of lncRNA function is associated with various human non-infectious diseases, such as inflammatory bowel disease, cardiovascular diseases, and diabetes mellitus. Here, we provide an overview of the regulation and mechanisms of lncRNA function in the development and differentiation of innate immune cells, and during the activation or repression of innate immune responses. These elucidations might be beneficial for the development of therapeutic strategies targeting inflammatory and innate immune-mediated diseases.
Yunhui Jia & Yuanyuan Wei. Modulators of MicroRNA Function in the Immune System.
Int. J. Mol. Sci. 2020; 21(7): 2357.

Yuanyuan Wei*, Aging's Accomplice in Harming the Cardiovascular System microRNA-217.

Arterioscler Thromb Vasc Biol. 2020; 40:2566–2568.

Atherosclerosis is a leading -but potentially preventable- cause of death and disability worldwide resulting in devastating diseases, such as myocardial infarction due to coronary artery disease or stroke. The current concept of atherogenesis includes a central role of apolipoprotein B-containing lipoproteins, such as LDL or remnant lipoproteins, which trigger a chronic inflammatory response of the vessel wall dominated by the  infiltration of monocyte-derived macrophages. Multiple stimuli, including cytokines, chemokines and modified lipoproteins, may dynamically modulate the macrophage phenotype in atherosclerotic lesions. Our lab aims to understand how macrophage phenotype is regulated during atherosclerosis progression, and figure out the potential therapeutic application of targeting macrophages in atherosclerosis.

Regulatory RNAs in macrophages and atherosclerosis

Our research has found that regulatory RNAs, such as miRNAs, play crucial roles in atherosclerosis by regulating macrophage polarization and metabolism. However, how regulatory RNA functions are modulated in macrophages  during atherosclerosis progression is still unknown.
Contribution of organelle interactions to macrophage functions
and atherosclerosis progression

It is known that organelles communicate witheach other to maintain cellular homeostasis. However, how signals are transduced among organelles to determine the immune functions of macrophages has not been clear yet.