Silencing Zonula occludens 2 (ZO-2), a tight junctions (TJ) scaffold protein, in epithelial cells (MDCK ZO-2 KD) triggers: 1) Decreased cell to substratum attachment, accompanied by reduced expression of claudin-7 and integrin β1, and increased vinculin recruitment to focal adhesions and stress fibers formation; 2) Lowered cell-cell aggregation and appearance of wider intercellular spaces; 3) Increased RhoA/ROCK activity, mediated by GEF-HI recruitment to cell borders by cingulin; 4) Increased Cdc42 activity, mitotic spindle disorientation and the appearance of cysts with multiple lumens; 5) Increased Rac and cofilin activity, multiple lamellipodia formation and random cell migration but increased wound closure; 6) Diminished cingulin phosphorylation and disappearance of planar network of microtubules at the TJ region; and 7) Increased transepithelial electrical resistance at steady state, coupled to an increased expression of ZO-1 and claudin-4 and a decreased expression of claudin-2 and paracingulin. Hence, ZO-2 is a crucial regulator of Rho proteins activity and the development of epithelial cytoarchitecture and barrier function.
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http://dx.doi.org/10.1016/j.bbamcr.2017.05.016 | DOI Listing |
Pituitary
January 2025
Departments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland.
Background: Arginine infusion stimulates copeptin secretion, a surrogate marker of arginine vasopressin (AVP), thereby serving as a diagnostic test in the differential diagnosis of suspected AVP deficiency (AVP-D). Yet, the precise mechanism underlying the stimulatory effect of arginine on the vasopressinergic system remains elusive. Arginine plays a significant role in the urea cycle and increases the production of urea.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Invasive Cardiology, Independent Public Specialist Western Hospital John Paul II, Lazarski University, 05-825 Grodzisk Mazowiecki, Poland.
Despite significant advances in imaging modalities for diagnosing coronary artery disease (CAD), there remains a need for novel diagnostic approaches with high predictive values and fewer limitations. Circulating biomarkers, including cytokines such as interleukin-6 (IL-6) and interleukin-8 (IL-8), cell adhesion molecules such as soluble vascular cell adhesion molecule-1 (sVCAM-1), peptides secreted by endothelial cells such as endothelin-1 (ET-1), and enzymes involved in extracellular matrix remodeling such as a disintegrin and metalloproteinase with thrombospondin motifs-1 (ADAMTS-1) offer a promising alternative. This study aimed to evaluate the correlation between the plasma levels of selected biomarkers and the presence and severity of CAD.
View Article and Find Full Text PDFGenes (Basel)
January 2025
The Cornea Dystrophy Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemungu, Seoul 03722, Republic of Korea.
(1) Background: The phenotypes of classic lattice corneal dystrophy (LCD) and granular corneal dystrophy type 2 (GCD2) that result from abnormalities in gene () have previously been described. The phenotype of compound heterozygous classic LCD and GCD2, however, has not yet been reported. (2) Case report: A 39-year-old male (proband) presented to our clinic complaining of decreased vision bilaterally.
View Article and Find Full Text PDFBiomolecules
December 2024
Cancer Metastasis Branch, Research Institute, National Cancer Center, Goyang 10408, Republic of Korea.
Metastatic cancer accounts for most cancer-related deaths, and identifying specific molecular targets that contribute to metastatic progression is crucial for the development of effective treatments. Hypoxia, a feature of solid tumors, plays a role in cancer progression by inducing resistance to therapy and accelerating metastasis. Here, we report that CCAAT/enhancer-binding protein beta (C/EBPβ) transcriptionally regulates () and thus promotes migration and invasion of non-small-cell lung cancer (NSCLC) cells under hypoxic conditions.
View Article and Find Full Text PDFBiomolecules
December 2024
Department of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515041, China.
RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form to the GDP-bound form. GAP has traditionally been known as a tumor suppressor. However, studies increasingly suggest that overexpressed RACGAP1 activates Rac and RhoA in multiple cancers to mediate downstream oncogene overexpression by assisting in the nuclear translocation of signaling molecules and to promote cytokinesis by regulating the cytoskeleton or serving as a component of the central spindle.
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