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        <title>Experimental Biology and Medicine | Cell and Developmental Biology section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/cell-and-developmental-biology</link>
        <description>RSS Feed for Cell and Developmental Biology section in the Experimental Biology and Medicine journal | New and Recent Articles</description>
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        <pubDate>2026-04-10T19:55:56.866+00:00</pubDate>
        <ttl>60</ttl>
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        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10321</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10321</link>
        <title><![CDATA[Coenzyme Q10 alleviates neurological deficits in a mouse model of intracerebral hemorrhage by reducing inflammation and apoptosis]]></title>
        <pubdate>2025-02-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaoqing Yang</author><author>Yi Zhao</author><author>Sisi Yu</author><author>Lihui Chi</author><author>Yeyan Cai</author>
        <description><![CDATA[This research study was directed towards to assessing whether coenzyme Q10 (CoQ10) is linked to neuroprotection and induces anti-inflammatory and anti-neuronal death responses in an Intracerebral hemorrhage (ICH) mouse model via right caudate nucleus injection with collagenase VII. Autologous blood was injected into mice to induce ICH. We found that FoxM1 was upregulated in the ICH-injured animals. Moreover, CoQ10 treatment effectively ameliorated neurological deficits, mitigated cerebral edema, and minimized hematoma in model mice, demonstrating dose-dependent efficacy and promoting the functional recovery of the animals. ELISA and real-time PCR assays of pro-inflammatory cytokines indicated that CoQ10 was capable of alleviating neuroinflammation in ICH. In line with the part of CoQ10 in attenuating the inflammatory response, CoQ10 also suppressed cell apoptosis in the ICH-injured brain, which partly accounts for its neuroprotective effect. Furthermore, our analysis of different inflammatory pathways indicated that CoQ10 targeted the nuclear factor-kappa B signaling axis. Our findings suggest that CoQ10 protects against ICH by mitigating neuroinflammatory responses and preventing neuronal apoptosis, with the underlying mechanism possibly being connected with nuclear factor-kappa B pathway regulation. Therefore, CoQ10 holds significant potential as a therapeutic strategy for treating ICH.]]></description>
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        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10377</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10377</link>
        <title><![CDATA[Baseline gene expression in BALB/c and C57BL/6 peritoneal macrophages influences but does not dictate their functional phenotypes]]></title>
        <pubdate>2025-01-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Carlos M. Restrepo</author><author>Alejandro Llanes</author><author>Lizzi Herrera</author><author>Esteban Ellis</author><author>Iliana Quintero</author><author>Patricia L. Fernández</author>
        <description><![CDATA[Macrophages are effector cells of the immune system and essential modulators of immune responses. Different functional phenotypes of macrophages with specific roles in the response to stimuli have been described. The C57BL/6 and BALB/c mouse strains tend to selectively display distinct macrophage activation states in response to pathogens, namely, the M1 and M2 phenotypes, respectively. Herein we used RNA-Seq and differential expression analysis to characterize the baseline gene expression pattern of unstimulated resident peritoneal macrophages from C57BL/6 and BALB/c mice. Our aim is to determine if there is a possible predisposition of these mouse strains to any activation phenotype and how this may affect the interpretation of results in studies concerning their interaction with pathogens. We found differences in basal gene expression patterns of BALB/c and C57BL/6 mice, which were further confirmed using RT-PCR for a subset of relevant genes. Despite these differences, our data suggest that baseline gene expression patterns of both mouse strains do not appear to determine by itself a specific macrophage phenotype.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10419</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10419</link>
        <title><![CDATA[Corrigendum: Decreased PPP1R3G in pre-eclampsia impairs human trophoblast invasion and migration via Akt/MMP-9 signaling pathway]]></title>
        <pubdate>2024-12-13T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Huimin Shi</author><author>Renyu Kong</author><author>Xu Miao</author><author>Lingshan Gou</author><author>Xin Yin</author><author>Yuning Ding</author><author>Xiliang Cao</author><author>Qingyong Meng</author><author>Maosheng Gu</author><author>Feng Suo</author>
        <description></description>
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        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10040</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10040</link>
        <title><![CDATA[Role of regulatory T cells in mouse lung development]]></title>
        <pubdate>2024-03-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jian-Feng Jiang</author><author>Hong-Yan Lu</author><author>Ming-Yan Wang</author><author>Lang-Yue He</author><author>Ying Zhu</author><author>Yu Qiao</author>
        <description><![CDATA[Regulatory T cells (Tregs) constitute a specialized subset of T cells with dual immunoregulatory and modulatory functions. Recent studies have reported that Tregs mediate immune responses and regulate the development and repair processes in non-lymphoid tissues, including bone and cardiac muscle. Additionally, Tregs facilitate the repair and regeneration of damaged lung tissues. However, limited studies have examined the role of Tregs in pulmonary development. This study aimed to evaluate the role of Tregs in pulmonary development by investigating the dynamic alterations in Tregs and their hallmark cellular factor Forkhead box P3 (Foxp3) at various stages of murine lung development and establishing a murine model of anti-CD25 antibody-induced Treg depletion. During the early stages of murine lung development, especially the canalicular and saccular stages, the levels of Treg abundance and expression of Foxp3 and transforming growth factor-β (TGF-β) were upregulated. This coincided with the proliferation period of alveolar epithelial cells and vascular endothelial cells, indicating an adaptation to the dynamic lung developmental processes. Furthermore, the depletion of Tregs disrupted lung tissue morphology and downregulated lung development-related factors, such as surfactant protein C (SFTPC), vascular endothelial growth factor A (VEGFA) and platelet endothelial cell adhesion molecule-1 (PECAM1/CD31). These findings suggest that Tregs promote murine lung development.]]></description>
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