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Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Capra hircus Mus musculus

PROVIDER: GSE212668 | GEO | 2023/09/01

REPOSITORIES: GEO

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Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [Dmrt1 RNA-Seq]

Project description:To explore the potential function of Dmrt1 in spermatogenesis, we constructed a Dmrt1-deficiency mouse model by knockdown Dmrt1 in testicular seminiferous tubule specifically

2023-09-01 | GSE212664 | GEO

Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [Spry1 KD RNA-Seq]

Project description:To explore the function of Spry1 in testis, we constructed a mouse model with testicular specific KD of Spry1 through seminiferous tubule transplantation

2023-09-01 | GSE212667 | GEO

Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [ChIP-Seq]

Project description:In order to explore the mechanisms of Dmrt1 in regulating testicular immune homeostasis, we performed ChIP-seq analysis on primary SCs infected with a lentiviral vector expressing FLAG-tagged Dmrt1

2023-09-01 | GSE212665 | GEO

Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway

Project description:Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway

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Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [Spry1 KD RNA-Seq]

Project description:Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [Spry1 KD RNA-Seq]

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Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [ChIP-Seq]

Project description:Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [ChIP-Seq]

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MicroRNA-21 maintains hematopoietic stem cell homeostasis through sustaining the NF-κB signaling pathway in mice.

Project description:Long-term hematopoietic output is dependent on hematopoietic stem cell (HSC) homeostasis which is maintained by a complex molecular network. Among these, microRNAs play crucial roles, while the underlying molecular basis has not been fully elucidated. Here, we show that miR-21 is enriched in murine HSCs, and mice with conditional knockout of miR-21 exhibit an obvious perturbation in normal hematopoiesis. Moreover, significant loss of HSC quiescence and long-term reconstituting ability are observed in the absence of miR-21. Further studies reveal that miR-21 deficiency markedly decreases the NF-κB pathway, accompanied by increased expression of PDCD4, a direct target of miR-21, in HSCs. Interestingly, overexpression of PDCD4 in wild-type HSCs generates similar phenotypes as those of miR-21-deficient HSCs. More importantly, knockdown of PDCD4 can significantly rescue the attenuation of NF-κB activity, thereby improving the defects in miR-21-null HSCs. On the other hand, we find that miR-21 is capable of preventing HSCs from ionizing radiation-induced DNA damage via activation of the NF-κB pathway. Collectively, our data demonstrate that miR-21 is involved in maintaining HSC homeostasis and function, at least in part, by regulating the PDCD4-mediated NF-κB pathway and provide a new insight into the radioprotection of HSCs.

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Dauricine Attenuates Vascular Endothelial Inflammation Through Inhibiting NF-κB Pathway.

Project description:Endothelial cells are the fundamental components of blood vessels that regulate several physiological processes including immune responses, angiogenesis, and vascular tone. Endothelial dysfunction contributes to the development of various diseases such as acute lung injury, and endothelial inflammation is a vital part of endothelial dysfunction. Dauricine is an extract isolated from Menispermum dauricum DC, a traditional Chinese medical plant that can be used for pharyngitis. In this work, we found that IL-1β-induced overexpression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin was inhibited by dauricine in primary human umbilical vein endothelial cells (HUVECs). Correspondingly, adhesion of human acute monocytic leukemia cell line (THP-1) to HUVECs was decreased by dauricine. Further studies showed that dauricine inhibited the activation of nuclear factor-κB (NF-κB) pathway in HUVECs stimulated with IL-1β. In vivo, dauricine protected mice from lipopolysaccharide (LPS)-induced acute lung injury. In lung tissues, the activation of NF-κB pathway and the expression of its downstream genes (ICAM-1, VCAM-1, and E-selectin) were decreased by dauricine, consistent with what was found in vitro. In summary, we concluded that dauricine could alleviate endothelial inflammation by suppressing NF-κB pathway, which might serve as an effective candidate for diseases related with endothelial inflammation.

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Caffeic acid phenethyl ester attenuates osteoarthritis progression by activating NRF2/HO‑1 and inhibiting the NF‑κB signaling pathway.

Project description:Osteoarthritis (OA) is the most common degenerative disease affecting the joints, and inflammation appears to play a critical role in the initiation and progression of OA. Caffeic acid phenethyl ester (CAPE), a natural flavonoid compound, has anti‑inflammatory and antioxidant functions. However, its anti‑inflammatory effects on OA and the underlying mechanisms of action of CAPE in the treatment of OA remain elusive. Therefore, the present study investigated the anti‑inflammatory effects of CAPE on IL‑1β‑stimulated chondrocytes in vitro and surgically induced rat models of OA in vivo. In vitro, CAPE reduced the expression of inducible nitric oxide synthase and cyclooxygenase‑2 in IL‑1β‑stimulated chondrocytes, as well as the extracellular secretion of nitric oxide and prostaglandin E2 in the cell culture supernatants. In addition, CAPE attenuated the degradation of extracellular matrix by increasing the expression of aggrecan and collagen II, and decreasing the expression of MMP3, MMP13 and a disintegrin and metalloproteinase with thrombospondin motif‑5. Furthermore, CAPE attenuated NF‑κB signaling and activated the nuclear factor erythroid 2‑related factor 2/heme oxygenase‑1 signaling pathway in IL‑1β‑stimulated chondrocytes. In vivo, CAPE protected cartilage from destruction and delayed the progression of OA in rats. Taken together, the findings of the present study indicated that CAPE may be a potential therapeutic agent for the prevention or treatment of OA.

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TRIM31 promotes glioma proliferation and invasion through activating NF-κB pathway.

Project description:BackgroundGlioma is the most lethal primary brain tumor, the survival rate still isn't improved in the past decades. It's essential to study the regulatory mechanism of glioma progression, hoping to find new therapy targets or methods. The family of tripartite motif (TRIM) containing proteins are E3 ubiquitination ligases, which play critical role in various tumor progression.MethodsCell proliferation and invasion were analyzed by colony formation assay, soft agar growth assay, BrdU incorporation assay and transwell invasion assay. Luciferase reporter analysis was used to analyze NF-κB pathway activity.ResultsWe found TRIM31 was upregulated in glioma cells and tissues, its overexpression significantly promoted glioma cell proliferation and invasion, while its knockdown significantly inhibited glioma cell proliferation and invasion. Mechanism analysis found TRIM31 promoted NF-κB pathway activity and increased its targets expression. NF-κB inhibition reversed the phenotype caused by TRIM31, confirming TRIM31 promoted glioma progression through activating NF-κB pathway. Using clinical specimens found TRIM31 expression was positively correlative with NF-κB activity.ConclusionThis study found TRIM31 promoted glioma proliferation and invasion through activating NF-κB activity.

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