Lipid rafts, also known as microdomains, are important components of cell membranes and are enriched in cholesterol, glycophospholipids and receptors. They are involved in various essential cellular processes, including endocytosis, exocytosis and cellular signaling. Receptors are concentrated at lipid rafts, through which cellular signaling can be transmitted. Pathogens exploit these signaling mechanisms to enter cells, proliferate and egress. However, lipid rafts also play an important role in initiating antimicrobial responses by sensing pathogens via clustered pathogen-sensing receptors and triggering downstream signaling events such as programmed cell death or cytokine production for pathogen clearance. In this review, we discuss how both host and pathogens use lipid rafts and associated proteins in an arms race to survive. Special attention is given to the involvement of the major vault protein, the main constituent of a ribonucleoprotein complex, which is enriched in lipid rafts upon infection with vaccinia virus.

/pdf/role-of-lipid-rafts-in-pathogen-host-interaction-a-mini-1nocx8aj.pdf

Role of Lipid Rafts in Pathogen-Host Interaction - A Mini Review

Temporomandibular joint osteoarthritis (TMJ OA) is a degenerative joint disease with no complete cure at present. Notably, the inflammatory microenvironment in TMJ OA is modulated by oxidative stress, which impacts cartilage metabolism, chondrocyte apoptosis, inflammatory cytokine release, and extracellular matrix (ECM) synthesis. Thus, it is reasoned that reducing excess reactive oxygen species (ROS) in the chondrocyte microenvironment may be an effective therapeutic strategy for TMJ OA. Recently, cascade nanozymes, including Pt@PCN222‐Mn, have been exploited to treat ROS‐associated diseases. Nevertheless, cascade nanozymes are not employed for TMJ OA therapy. To fill this gap, it is explored whether the Pt@PCN222‐Mn cascade nanozyme could be applied to the treatment of TMJ OA. The in vitro results demonstrate that the Pt@PCN222‐Mn nanozyme can inhibit the production of inflammatory factors, the degradation of ECM, and the apoptosis of chondrocytes by inhibiting the ROS‐nuclear factor kappa‐B (NF‐κB_ and mitogen‐activated protein kinase signaling pathways. The in vivo results further demonstrate that the Pt@PCN222‐Mn nanozyme can delay the progression of TMJ OA in the rat unilateral anterior crossbite model. It is believed that insightful perspectives on the application of nanozymes in TMJ OA will be provided here.

Integrated Cascade Nanozyme Remodels Chondrocyte Inflammatory Microenvironment in Temporomandibular Joint Osteoarthritis via Inhibiting ROS‐NF‐κB and MAPK Pathways

Osteoclast-mediated excessive bone resorption was highly related to diverse bone diseases including osteoporosis. BRISC and BRCA1-A complex member 2 (Babam2) was an evolutionarily conserved protein that is highly expressed in bone tissues. However, whether Babam2 is involved in osteoclast formation is still unclear. In this study, we identify Babam2 as an essential negative regulator of osteoclast formation. We demonstrate that Babam2 knockdown significantly accelerated osteoclast formation and activity, while Babam2 overexpression blocked osteoclast formation and activity. Moreover, we demonstrate that the bone resorption activity was significantly downregulated in Babam2-transgenic mice as compared with wild-type littermates. Consistently, the bone mass of the Babam2-transgenic mice was increased. Furthermore, we found that Babam2-transgenic mice were protected from LPS-induced bone resorption activation and thus reduced the calvarial bone lesions. Mechanistically, we demonstrate that the inhibitory effects of Babam2 on osteoclast differentiation were dependent on Hey1. As silencing Hey1 largely diminished the effects of Babam2 on osteoclastogenesis. Finally, we show that Babam2 interacts with Hey1 to inhibit Nfatc1 transcription. In sum, our results suggested that Babam2 negatively regulates osteoclastogenesis and bone resorption by interacting with Hey1 to inhibit Nfatc1 transcription. Therefore, targeting Babam2 may be a novel therapeutic approach for osteoclast-related bone diseases.

/pdf/babam2-negatively-regulates-osteoclastogenesis-by-1jnhy6k9.pdf

Babam2 negatively regulates osteoclastogenesis by interacting with Hey1 to inhibit Nfatc1 transcription

http://manuscript.elsevier.com/S0955067422000023/pdf/S0955067422000023.pdf

Plasmalemmal interface for calcium signaling in osteoclast differentiation.

Isoimperatorin attenuates bone loss by inhibiting the binding of RANKL to RANK.

Rationale: Bone homeostasis is maintained by a balanced interplay of osteoblasts and osteoclasts. Osteoclasts are derived from monocyte/macrophage lineage. Major vault protein (MVP) is known to promote apoptosis and prevent metabolic diseases in macrophage. However, whether MVP is involved in osteoclastogenesis is unknown. Here, we identified an important function of MVP as a negative regulator of osteoclastogenesis and its therapeutic potential in preventing bone loss. Methods: Expression of MVP in osteoclasts was investigated in human tumor tissues with immunohistochemical staining. Next, we generated total body (Mvp-/- ) and monocyte-specific (Mvpf/fLyz2-Cre) MVP gene knockout mice to observe bone phenotype and osteoclastogenesis using micro-CT and bone histomorphometry. Moreover, we examined the effects of MVP on osteoclast differentiation, bone resorption, NFATc1 activation and calcium oscillations in vitro. Finally, we explored the clinical potential of targeting MVP in two osteoporosis mouse models and used an adeno-associated virus (AAV) gene to overexpress MVP locally in mice. Results: We found that Mvp-/- and Mvpf/fLyz2-Cre mice both exhibited osteoporosis-like phenotypes. MVP-deficiency also enhanced calcineurin-NFATc1 signaling and promoted NFATc1 activity, which led to enhanced osteoclastogenesis and bone resorption. Calcineurin inhibition using the small molecule inhibitor FK506 corrected the enhanced osteoclastogenesis in Mvpf/fLyz2-Cre group. Additionally, MVP reexpression in Mvpf/fLyz2-Cre group rescued calcineurin expression. MVP overexpression in wild-type mice prevented pathologic bone loss in mouse models of ovariectomized (OVX) and calvaria-adjacent lipopolysaccharide (LPS)-injected. Conclusions: Our data suggested that MVP negatively regulates osteoclast differentiation and bone resorption via inhibition of calcineurin-NFATc1 signaling. In osteoclast-related bone diseases such as osteoporosis, manipulation of MVP activity may be an attractive therapeutic target.

Major vault protein (MVP) negatively regulates osteoclastogenesis via calcineurin-NFATc1 pathway inhibition.

Shang-Ke-Huang-Shui and coptisine alleviate osteoarthritis in the knee of monosodium iodoacetate-induced rats through inhibiting CXCR4 signaling.

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Major vault protein (MVP) negatively regulates osteoclastogenesis via calcineurin-NFATc1 pathway inhibition.

Shang-Ke-Huang-Shui and coptisine alleviate osteoarthritis in the knee of monosodium iodoacetate-induced rats through inhibiting CXCR4 signaling.