Tmem161a regulates bone formation and bone strength through the P38 MAPK pathway

Nagai, Takuya; Sekimoto, Tomohisa; Kurogi, Syuji; Ohta, Tomomi; Miyazaki, Shihoko; Yamaguchi, Yoichiro; Tajima, Takuya; Chosa, Etsuo; Imasaka, Mai; Yoshinobu, Kumiko; Araki, Kimi; Araki, Masatake; Choijookhuu, Narantsog; Sato, Katsuaki; Hishikawa, Yoshitaka; Funamoto, Taro

doi:10.1038/s41598-023-41837-4

Cited by 5 publications

(3 citation statements)

References 45 publications

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“…p38 MAPK signaling pathway is essential for bone formation and bone strength in vivo. 52 , 53 The p38 MAPK pathway also plays a central role in the regulation of monocyte/macrophage development and differentiation. 54 – 57 To validate the mechanism of Tim4-regulated CD301b + macrophages phenotype, we focused on p38 MAPK signaling pathway because evidences have described that Tim4 in macrophages could mediate p38 MAPK signaling pathway and might facilitate tissue regeneration.…”

Section: Discussionmentioning

confidence: 99%

Tim4 deficiency reduces CD301b+ macrophage and aggravates periodontitis bone loss

Wang,

Zeng,

Wang

et al. 2024

Int J Oral Sci

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Periodontitis is a common chronic inflammatory disease that causes the periodontal bone destruction and may ultimately result in tooth loss. With the progression of periodontitis, the osteoimmunology microenvironment in periodontitis is damaged and leads to the formation of pathological alveolar bone resorption. CD301b+ macrophages are specific to the osteoimmunology microenvironment, and are emerging as vital booster for conducting bone regeneration. However, the key upstream targets of CD301b+ macrophages and their potential mechanism in periodontitis remain elusive. In this study, we concentrated on the role of Tim4, a latent upstream regulator of CD301b+ macrophages. We first demonstrated that the transcription level of Timd4 (gene name of Tim4) in CD301b+ macrophages was significantly upregulated compared to CD301b− macrophages via high-throughput RNA sequencing. Moreover, several Tim4-related functions such as apoptotic cell clearance, phagocytosis and engulfment were positively regulated by CD301b+ macrophages. The single-cell RNA sequencing analysis subsequently discovered that Cd301b and Timd4 were specifically co-expressed in macrophages. The following flow cytometric analysis indicated that Tim4 positive expression rates in total macrophages shared highly synchronized dynamic changes with the proportions of CD301b+ macrophages as periodontitis progressed. Furthermore, the deficiency of Tim4 in mice decreased CD301b+ macrophages and eventually magnified alveolar bone resorption in periodontitis. Additionally, Tim4 controlled the p38 MAPK signaling pathway to ultimately mediate CD301b+ macrophages phenotype. In a word, Tim4 might regulate CD301b+ macrophages through p38 MAPK signaling pathway in periodontitis, which provided new insights into periodontitis immunoregulation as well as help to develop innovative therapeutic targets and treatment strategies for periodontitis.

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Section: Discussionmentioning

confidence: 99%

Tim4 deficiency reduces CD301b+ macrophage and aggravates periodontitis bone loss

Wang,

Zeng,

Wang

et al. 2024

Int J Oral Sci

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“…The overexpression of StTMEM161A leads to reduced levels of oxidant-induced DNA damage and apoptosis. Previous study indicated that TMEM161A plays a role in protecting against oxidative stress [57]. This gene is activated by calcium as a chloride channel.…”

Section: Wgcna Analysis For Pvy Resistancementioning

confidence: 99%

Genotyping-by-sequencing and weighted gene co-expression network analysis of genes responsive against Potato virus Y in commercial potato cultivars

Hajibarat,

Saidi,

Zeinalabedini

et al. 2024

PLoS ONE

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Potato is considered a key component of the global food system and plays a vital role in strengthening world food security. A major constraint to potato production worldwide is the Potato Virus Y (PVY), belonging to the genus Potyvirus in the family of Potyviridae. Selective breeding of potato with resistance to PVY pathogens remains the best method to limit the impact of viral infections. Understanding the genetic diversity and population structure of potato germplasm is important for breeders to improve new cultivars for the sustainable use of genetic materials in potato breeding to PVY pathogens. While, genetic diversity improvement in modern potato breeding is facing increasingly narrow genetic basis and the decline of the genetic diversity. In this research, we performed genotyping-by-sequencing (GBS)-based diversity analysis on 10 commercial potato cultivars and weighted gene co-expression network analysis (WGCNA) to identify candidate genes related to PVY-resistance. WGCNA is a system biology technique that uses the WGCNA R software package to describe the correlation patterns between genes in multiple samples. In terms of consumption, these cultivars are a high rate among Iranian people. Using population structure analysis, the 10 cultivars were clustered into three groups based on the 118343 single nucleotide polymorphisms (SNPs) generated by GBS. Read depth ranged between 5 and 18. The average data size and Q30 of the reads were 145.98 Mb and 93.63%, respectively. Based on the WGCNA and gene expression analysis, the StDUF538, StGTF3C5, and StTMEM161A genes were associated with PVY resistance in the potato genome. Further, these three hub genes were significantly involved in defense mechanism where the StTMEM161A was involved in the regulation of alkalization apoplast, the StDUF538 was activated in the chloroplast degradation program, and the StGTF3C5 regulated the proteins increase related to defense in the PVY infected cells. In addition, in the genetic improvement programs, these hub genes can be used as genetic markers for screening commercial cultivars for PVY resistance. Our survey demonstrated that the combination of GBS-based genetic diversity germplasm analysis and WGCNA can assist breeders to select cultivars resistant to PVY as well as help design proper crossing schemes in potato breeding.

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“…The sections were deparaffinized with toluene and rehydrated using a graded ethanol series, and then autoclaved at 120C for 15 min in 10-mM citrate buffer (pH 6.0). 19,20 After inhibition of endogenous peroxidase activity with 3% H 2 O 2 in methanol for 30 min, the sections were preincubated with 500-µg/ml normal goat IgG and 1% BSA in PBS for 1 hr to block nonspecific binding of antibodies. The sections were then reacted with the following primary antibodies for 16-17 hr: anti-HMGB2 (cat.…”

Section: Animals and Tissue Preparationmentioning

confidence: 99%

HMGB2 Promotes De Novo Lipogenesis to Accelerate Hepatocyte Proliferation During Liver Regeneration

Choijookhuu,

Yano,

Lkham-Erdene

et al. 2024

J Histochem Cytochem.

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Liver regeneration is a well-orchestrated compensatory process that is regulated by multiple factors. We recently reported the importance of the chromatin protein, a high-mobility group box 2 (HMGB2) in mouse liver regeneration. However, the molecular mechanism remains unclear. In this study, we aimed to study how HMGB2 regulates hepatocyte proliferation during liver regeneration. Seventy-percent partial hepatectomy (PHx) was performed in wild-type (WT) and HMGB2-knockout (KO) mice, and the liver tissues were used for microarray, immunohistochemistry, quantitative polymerase chain reaction (qPCR), and Western blotting analyses. In the WT mice, HMGB2-positive hepatocytes colocalized with cell proliferation markers. In the HMGB2-KO mice, hepatocyte proliferation was significantly decreased. Oil Red O staining revealed the transient accumulation of lipid droplets at 12–24 hr after PHx in the WT mouse livers. In contrast, decreased amount of lipid droplets were found in HMGB2-KO mouse livers, and it was preserved until 36 hr. The microarray, immunohistochemistry, and qPCR results demonstrated that the expression of lipid metabolism–related genes was significantly decreased in the HMGB2-KO mouse livers. The in vitro experiments demonstrated that a decrease in the amount of lipid droplets correlated with decreased cell proliferation activity in HMGB2-knockdown cells. HMGB2 promotes de novo lipogenesis to accelerate hepatocyte proliferation during liver regeneration:

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Tmem161a regulates bone formation and bone strength through the P38 MAPK pathway

Cited by 5 publications

References 45 publications

Tim4 deficiency reduces CD301b+ macrophage and aggravates periodontitis bone loss

Tim4 deficiency reduces CD301b+ macrophage and aggravates periodontitis bone loss

Genotyping-by-sequencing and weighted gene co-expression network analysis of genes responsive against Potato virus Y in commercial potato cultivars

HMGB2 Promotes De Novo Lipogenesis to Accelerate Hepatocyte Proliferation During Liver Regeneration

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