TIPE1 accelerates atherogenesis by inducing endothelial dysfunction in response to oxidative stress.

Atherosclerosis is an inflammatory disease of the arterial wall, which involves endothelial cells and immune cells. Endothelial dysfunction has been considered an important step in the initiation of the disease. TIPE1 is a newly identified protein of the TIPE family, and plays a vital role in inflammation and tumorigenesis.

Clinical Significance of TIPE2 Protein Upregulation in Non-Hodgkin's Lymphoma.

Non-Hodgkin's lymphoma (NHL), which includes diffuse large B-cell lymphoma (DLBCL) and peripheral T-cell lymphoma, is a refractory malignant tumor originated from the lymphatic system. TNFAIP8L2 (TIPE2 or tumor necrosis-alpha-induced protein-8 like 2) is a negative regulator for inflammation and an inhibitor for carcinogenesis. However, whether TIPE2 plays a role in lymphomagenesis is unknown.

TIPE2 protein prevents injury-induced restenosis in mice.

Proliferation of vascular smooth muscle cells (VSMCs) plays an important role in restenosis, a disease characterized by smooth muscle cell hyperplasia and neointimal formation. How proliferation signals are controlled to avoid restenosis is not fully understood. Here we report that TIPE2, the tumor necrosis factor (TNF) α-induced protein 8-like 2 (TNFAIP8L2), suppresses injury-induced restenosis by inhibiting VSMCs proliferation.

TIPE2 negatively regulates inflammation by switching arginine metabolism from nitric oxide synthase to arginase.

TIPE2, the tumor necrosis factor (TNF)-alpha-induced protein 8-like 2 (TNFAIP8L2), plays an essential role in maintaining immune homeostasis. It is highly expressed in macrophages and negatively regulates inflammation through inhibiting Toll-like receptor signaling. In this paper, we utilized RAW264.

TIPE2 deficiency accelerates neointima formation by downregulating smooth muscle cell differentiation.

Phenotypic switching of vascular smooth muscle cells (VSMCs) is known to play a key role in the development of atherosclerosis. However, the mechanisms that mediate VSMC phenotypic switching are unclear. We report here that TIPE2, the tumor necrosis factor (TNF) α-induced protein 8-like 2 (TNFAIP8L2), plays an atheroprotective role by regulating phenotypic switching of VSMCs in response to oxidized low-density lipoprotein (ox-LDL) stimuli.