Cell cultures of Mandevilla velutina have proved to be an interesting production system for biomass and secondary metabolites able to inhibit the hypotensive activity of bradykinin, a nonapeptide generated in plasma during tissue trauma. The crude ethyl acetate extract of cultured cells contains about 31- to 79-fold more potent anti-bradykinin compounds (e.g., velutinol A) than that obtained with equivalent extracts of tubers. Somaclonal variation may be an explanation for the wide range of inhibitor activity found in the cell cultures. The heterogeneity concerning morphology, differentiation, carbon dissimilation, and velutinol A production in M. velutina cell cultures is reported. Cell cultures showed an asynchronous growth and cells in distinct developmental stages. Meristematic cells were found as the major type, with several morphological variations. Cell aggregates consisting only of meristematic cells, differentiated cells containing specialized cell structures such as functional chloroplasts (cytodifferentiation) and cells with embryogenetic characteristics were observed. The time course for sucrose metabolism indicated cell populations with significant differences in growth and metabolic rates, with the highest biomass-producing cell line showing a cell cycle 60% shorter and a metabolic rate 33.6% higher than the control (F2 cell population). MALDI-TOF mass spectrometric analysis of velutinol A in selected cell lines demonstrated the existence of velutinol A producing and nonproducing somaclones. These results point to a high genetic heterogeneity in general and also in terms of secondary metabolite content.
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http://dx.doi.org/10.1590/s0100-879x2002000600002 | DOI Listing |
Environ Sci Technol
January 2025
Department of Chemical Engineering and Applied Chemistry, University of Toronto, Toronto, Ontario M5S 3E5, Canada.
Benzene degradation under anoxic conditions was first reported more than 25 years ago; however, the activation mechanism in the absence of oxygen remains elusive. Progress has been hindered by the difficulty in cultivating anaerobic benzene-degrading enrichment cultures. Our laboratory has sustained a methanogenic enrichment culture harboring ORM2, a benzene fermenter distinct from any known genus but related to other known or predicted benzene degraders.
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December 2024
Michigan Alzheimer's Disease Research Center, Ann Arbor, MI, USA.
Background: Non-coding RNA species, such as microRNA (miRNA), regulate multiple biological and pathological processes by binding to target mRNAs and facilitating alteration of translation levels via complexes such as RNA-induced silencing complex (RISC). Disrupting this process could contribute to AD pathogenesis by fostering aggregation of hyperphosphorylated microtubule-associated protein tau and amyloid-β (Aβ) peptides, and neuroinflammation. Understanding how these pathological changes are regulated remains our research focus.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by synapse and memory failure, and severe cognitive impairment. Physical exercise stimulates neuroprotective pathways, has pro-cognitive actions, and has been reported to alleviate memory impairment in AD. Irisin, an exercise-induced hormone, is secreted following proteolytic cleavage of fibronectin type-III-domain-containing 5 (FNDC5).
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December 2024
University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
Karolinska Institutet, Solna, Sweden.
Background: Signal Peptide Peptidase-Like 2b (SPPL2b) is relevant for AD, being a brain-specific intramembrane protein involved in the cleavage of Alzheimer's disease (AD)-related proteins, such as BRI2, inflammatory-related proteins like CD74, TNFalpha, and Clec7a, and synaptic proteins Neuregulin-1 and VAMP 1-4. SPPL2b is specifically expressed in the hippocampus and cortex. The cleavage of TNFalpha by SPPL2b promotes the inflammatory pathway.
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