Aim: This study is aimed at identifying genetic and epigenetic crosstalk molecules and their target drugs involved in the interaction between neural stem/progenitor cells (NSPCs) and endothelial cells (ECs).
Materials And Methods: Datasets pertaining to reciprocal mRNA and noncoding RNA changes induced by the interaction between NSPCs and ECs were obtained from the GEO database. Differential expression analysis (DEA) was applied to identify NSPC-induced EC alterations by comparing the expression profiles between monoculture of ECs and ECs grown in EC/NSPC cocultures. DEA was also utilized to identify EC-induced NSPC alterations by comparing the expression profiles between monoculture of NSPCs and NSPCs grown in EC/NSPC cocultures. The DEGs and DEmiRNAs shared by NSPC-induced EC alterations and EC-induced NSPC alterations were then identified. Furthermore, miRNA crosstalk analysis and functional enrichment analysis were performed, and the relationship between DEmiRNAs and small molecular drug targets/environment chemical compounds was investigated.
Results: One dataset (GSE29759) was included and analyzed in this study. Six genes (i.e., MMP14, TIMP3, LOXL1, CCK, SMAD6, and HSPA2), three miRNAs (i.e., miR-210, miR-230a, and miR-23b), and three pathways (i.e., Akt, ERK1/2, and BMPs) were identified as crosstalk molecules. Six small molecular drugs (i.e., deptropine, fluphenazine, lycorine, quinostatin, resveratrol, and thiamazole) and seven environmental chemical compounds (i.e., folic acid, dexamethasone, choline, doxorubicin, thalidomide, bisphenol A, and titanium dioxide) were identified to be potential target drugs of the identified DEmiRNAs.
Conclusion: To conclude, three miRNAs (i.e., miR-210, miR-230a, and miR-23b) were identified to be crosstalks linking the interaction between ECs and NSPCs by implicating in both angiogenesis and neurogenesis. These crosstalk molecules might provide a basis for devising novel strategies for fabricating neurovascular models in stem cell tissue engineering.
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http://dx.doi.org/10.1155/2020/6630659 | DOI Listing |
Cell Commun Signal
January 2025
Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, No. 25, Taiping Road, Lu Zhou, Luzhou, Sichuan, 646000, China.
This review comprehensively explores the critical role of calcium as an essential small-molecule biomessenger in skeletal muscle function. Calcium is vital for both regulating muscle excitation-contraction coupling and for the development, maintenance, and regeneration of muscle cells. The orchestrated release of calcium from the endoplasmic reticulum (ER) is mediated by receptors such as the ryanodine receptor (RYR) and inositol 1,4,5-trisphosphate receptor (IP3R), which is crucial for skeletal muscle contraction.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Experimental Allergology and Immunology, Medical University of Bialystok, Bialystok, Poland.
The European Commission authorized the use of dried yellow mealworm (Tenebrio molitor - TM) as a food ingredient under Regulation EU 2021/882. As TM emerges as an important allergen source, sensitization and allergy to TM in various populations need investigation. The aim of this study was to assess the incidence of sensitization to TM before its introduction as a food ingredient in Poland, as well as checking the occurrence of co-sensitivity to TM and other invertebrate allergenic extracts and molecules.
View Article and Find Full Text PDFAnal Chim Acta
January 2025
College of Tobacco Science, Henan Agricultural University, Zhengzhou, 450046, China. Electronic address:
Background: Nitroxyl (HNO) is an emerging signaling molecule that plays a significant regulatory role in various aspects of plant biology, including stress responses and developmental processes. However, understanding the precise actions of HNO in plants has been challenging due to the absence of highly sensitive and real-time in situ monitoring tools. Consequently, it is crucial to develop effective and accurate detection methods for HNO.
View Article and Find Full Text PDFJ Phys Chem Lett
January 2025
Department of Chemistry, University of Hawai'i at Ma̅noa, Honolulu, Hawaii 96822, United States.
What if an experiment could combine the power of cycloaddition and cross-coupling with the formation of an aromatic molecule in a single collision? Crossed molecular beam experiments augmented with electronic structure and statistical calculations provided compelling evidence on a novel radical route involving 1,3-butadiynyl (HCCCC; X∑) radicals synthesizing (substituted) arylacetylenes in the gas phase upon reactions with 1,3-butadiene (CHCHCHCH; XA) and 2-methyl-1,3-butadiene (isoprene; CHC(CH)CHCH; XA'). This elegant mechanism merges two previously disconnected concepts of cross-coupling and cycloaddition-aromatization in a single collision event via the formation of two new C(sp)-C(sp) bonds and bending the 180° moiety of the linear 1,3-butadiynyl radical out of the ordinary by 60° to 120°. In addition to its importance to fundamental organic chemistry, this unconventional mechanism links two previously separated routes of gas-phase molecular mass growth processes of polyacetylenes and polycyclic aromatic hydrocarbons (PAHs), respectively, in low-temperature environments such as in cold molecular clouds like the Taurus Molecular Cloud (TMC-1) and in hydrocarbon-rich atmospheres of planets and their moons such as Titan, which revises the established understanding of low-temperature molecular mass growth processes in the Universe.
View Article and Find Full Text PDFACS Chem Neurosci
January 2025
Department of Life Sciences, Chalmers University of Technology, 412 96 Gothenburg, Sweden.
Amyloid fibrils are protein polymers noncovalently assembled through β-strands arranged in a cross-β structure. Biological amyloids were considered chemically inert until we and others recently demonstrated their ability to catalyze chemical reactions in vitro. To further explore the functional repertoire of amyloids, we here probe if fibrils of α-synuclein (αS) display chemical reactivity toward DNA.
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