Myeloid-derived growth factor promotes M2 macrophage polarization and attenuates Sjögren's syndrome via suppression of the CX3CL1/CX3CR1 axis.

Introduction: Primary Sjögren syndrome (pSS) is a systemic autoimmune disease that is characterized by the infiltration of immune cells into the salivary glands. The re-establishment of salivary glands (SGs) function in pSS remains a clinical challenge. Myeloid-derived growth factor (MYDGF) has anti-inflammatory, immunomodulatory, and tissue-functional restorative abilities.

Myeloid-derived growth factor ameliorates dextran sodium sulfate-induced colitis by regulating macrophage polarization.

Inflammatory bowel disease (IBD) is characterized by inflammatory conditions in the gastrointestinal tract. According to reports, IBD prevalence is increasing globally, with heavy economic and physical burdens. Current IBD clinical treatment is limited to pharmacological methods; therefore, new strategies are needed.

Dental pulp stem cells accelerate wound healing through CCL2-induced M2 macrophages polarization.

The crosstalk between mesenchymal stem cells (MSCs) and the host immune function plays a key role in the efficiency of tissue regeneration and wound healing. However, the difference in immunological modulation and tissue regeneration function between MSCs from different sources remains unclear. Compared to PDLSCs, BMMSCs, and ADSCs, DPSCs exhibited greater tissue regeneration potential and triggered more M2 macrophages .

The NF-κB pathway plays a vital role in rat salivary gland atrophy model.

Objective: The aim of this study was to explore the histopathological and genetic changes in the submandibular glands after duct ligation and provide important clues to functional regeneration.

Design: We established a rat salivary gland duct ligation model and observed pathological changes in the rat submandibular gland on day 1 and weeks 1, 2, 3, and 4 using hematoxylin and eosin staining, Alcian blue-periodic acid Schiff staining, Masson staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), and immunohistochemical staining. RNA sequencing was performed on normal salivary glands and those from the ligation model after 1 week.

Transient Activation of Hedgehog Signaling Inhibits Cellular Senescence and Inflammation in Radiated Swine Salivary Glands through Preserving Resident Macrophages.

Salivary gland function is commonly and irreversibly damaged by radiation therapy for head and neck cancer. This damage greatly decreases the patient's quality of life and is difficult to remedy. Previously, we found that the transient activation of Hedgehog signaling alleviated salivary hypofunction after radiation in both mouse and pig models through the inhibition of radiation-induced cellular senescence that is mediated by resident macrophages in mouse submandibular glands.

Total body irradiation-induced colon damage is prevented by nitrate-mediated suppression of oxidative stress and homeostasis of the gut microbiome.

Inorganic dietary nitrate plays vital roles in biological functions via the exogenous NO3/NO2/NO pathway under hypoxia and ischemia. We previously verified the antioxidative effects of inorganic nitrate in a mouse model of total body irradiation (TBI). Accordingly, in this study, we evaluated the effects of inorganic nitrate on prevention of TBI-induced colon injury and dysbiosis of the gut microbiome.

Silencing of CCR7 inhibits the growth, invasion and migration of prostate cancer cells induced by VEGFC.

Early in prostate cancer development, tumor cells express vascular endothelial growth factor C (VEGF-C), a secreted molecule that is important in angiogenesis progression. CC-chemokine receptor 7 (CCR7), another protein involved in angiogenesis, is strongly expressed in most human cancers, where it activated promotes tumor growth as well as favoring tumor cell invasion and migration. The present study aimed to investigate the effect of down-regulating CCR7 expression on the growth of human prostate cancer cells stimulated by VEGFC.