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"Ram, A."
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Plant terpenes: defense responses, phylogenetic analysis, regulation and clinical applications
The terpenoids constitute the largest class of natural products and many interesting products are extensively applied in the industrial sector as flavors, fragrances, spices and are also used in perfumery and cosmetics. Many terpenoids have biological activities and also used for medical purposes. In higher plants, the conventional acetate-mevalonic acid pathway operates mainly in the cytosol and mitochondria and synthesizes sterols, sesquiterpenes and ubiquinones mainly. In the plastid, the non-mevalonic acid pathway takes place and synthesizes hemi-, mono-, sesqui-, and diterpenes along with carotenoids and phytol tail of chlorophyll. In this review paper, recent developments in the biosynthesis of terpenoids, indepth description of terpene synthases and their phylogenetic analysis, regulation of terpene biosynthesis as well as updates of terpenes which have entered in the clinical studies are reviewed thoroughly.
Journal Article
Ēn̲ Periyār ? = Yaen Periyar ? : er̲pum mar̲uppum
Critical articles on E.V. Ramaswami Naicker, 1878-1973, social reformer from Tamil Nadu, India; previously published in English by \"The Wire\", an internet magazine.
Membrane transporters: the key drivers of transport of secondary metabolites in plants
Key messageThis review summarizes the recent updates in the area of transporters of plant secondary metabolites, including their applied aspects in metabolic engineering of economically important secondary metabolites.Plants have evolved biosynthetic pathways to produce structurally diverse secondary metabolites, which serve distinct functions, including defense against pathogens and herbivory, thereby playing a pivotal role in plant ecological interactions. These compounds often display interesting bioactivities and, therefore, have been used as repositories of natural drugs and phytoceuticals for humans. At an elevated level, plant secondary metabolites could be cytotoxic to the plant cell itself; therefore, plants have developed sophisticated mechanisms to sequester these compounds to prevent cytotoxicity. Many of these valuable natural compounds and their precursors are biosynthesized and accumulated at diverse subcellular locations, and few are even transported to sink organs via long-distance transport, implying the involvement of compartmentalization via intra- and intercellular transport mechanisms. The transporter proteins belonging to different families of transporters, especially ATP binding cassette (ABC) and multidrug and toxic compound extrusion (MATE) have been implicated in membrane-mediated transport of certain plant secondary metabolites. Despite increasing reports on the characterization of transporter proteins and their genes, our knowledge about the transporters of several medicinally and economically important plant secondary metabolites is still enigmatic. A comprehensive understanding of the molecular mechanisms underlying the whole route of secondary metabolite transportome, in addition to the biosynthetic pathways, will aid in systematic and targeted metabolic engineering of high-value secondary metabolites. The present review embodies a comprehensive update on the progress made in the elucidation of transporters of secondary metabolites in view of basic and applied aspects of their transport mechanism.
Journal Article
Tumour-vasculature development via endothelial-to-mesenchymal transition after radiotherapy controls CD44v6+ cancer cell and macrophage polarization
It remains controversial whether targeting tumour vasculature can improve radiotherapeutic efficacy. We report that radiation-induced endothelial-to-mesenchymal transition (EndMT) leads to tumour vasculature with abnormal SMA
+
NG2
+
pericyte recruitment during tumour regrowth after radiotherapy.
Trp53
(but not
Tgfbr2
) deletion in endothelial cells (ECs) inhibited radiation-induced EndMT, reducing tumour regrowth and metastases with a high CD44v6
+
cancer-stem-cell (CSC) content after radiotherapy. Osteopontin, an EndMT-related angiocrine factor suppressed by EC-
Trp53
deletion, stimulated proliferation in dormant CD44v6
+
cells in severely hypoxic regions after radiation. Radiation-induced EndMT significantly regulated tumour-associated macrophage (TAM) polarization. CXCR4 upregulation in radioresistant tumour ECs was highly associated with SDF-1
+
TAM recruitment and M2 polarization of TAMs, which was suppressed by
Trp53
deletion. These EndMT-related phenomena were also observed in irradiated human lung cancer tissues. Our findings suggest that targeting tumour EndMT might enhance radiotherapy efficacy by inhibiting the re-activation of dormant hypoxic CSCs and promoting anti-tumour immune responses.
Radiotherapy is the main treatment for most cancer, but it is unclear if targeting tumour vasculature can enhance tumour radiosensitivity. Here, the authors show that tumour endothelial-mesenchymal transition after radiotherapy leads to proliferation of radioresistant CSCs and tumour associated macrophages polarization.
Journal Article
Differential impact of top-down and bottom-up forces in structuring freshwater bacterial communities
Limited data exist on the simultaneous impact of bottom-up (nutrients) and top-down (viruses and heterotrophic nanoflagellates) forces in shaping freshwater bacterial communities. In our laboratory microcosms, nutrient additions (organic and inorganic) and viral reduction approach led to the proliferation of high nucleic acid (HNA) bacterial subpopulation without an increase in phage abundance. High viral-mediated bacterial lysis in the presence of nanoflagellates yielded high proportion of low nucleic acid bacterial subpopulation. 16S rRNA gene sequence analysis indicated that members of classes Proteobacteria and Bacteroidetes evoked differential responses to nutrients and mortality forces, thereby resulting in differences (P < 0.001) in bacterial community composition and diversity, as observed from analysis of similarities and UniFrac analysis. Bacterial species richness (Chao) and diversity (Shannon) index was significantly higher (P < 0.001) in the presence of both the top-down factors and viruses alone, whereas lower host diversity was observed under nutrient relaxation of growth-limiting substrates due to the explosive growth of opportunistic HNA bacterial subpopulation. Our results are in agreement with the theoretical model of ‘killing the winner’, where the availability of growth-limiting substrates can act as a stimulating factor for host community composition while top-down forces can operate in the control of host diversity.
Journal Article
Faecalibacterium prausnitzii alleviates inflammatory arthritis and regulates IL-17 production, short chain fatty acids, and the intestinal microbial flora in experimental mouse model for rheumatoid arthritis
Background
Rheumatoid arthritis (RA) is a systemic chronic inflammatory disease that leads to joint destruction and functional disability due to the targeting of self-antigens present in the synovium, cartilage, and bone. RA is caused by a number of complex factors, including genetics, environment, dietary habits, and altered intestinal microbial flora. Microorganisms in the gut bind to nod-like receptors and Toll-like receptors to regulate the immune system and produce various metabolites, such as short-chain fatty acids (SCFAs) that interact directly with the host.
Faecalibacterium prausnitzii
is a representative bacterium that produces butyrate, a well-known immunomodulatory agent in the body, and this microbe exerts anti-inflammatory effects in autoimmune diseases.
Methods
In this study,
F. prausnitzii
was administered in a mouse model of RA, to investigate RA pathology and changes in the intestinal microbial flora. Using collagen-induced arthritic mice, which is a representative animal model of RA, we administered
F. prausnitzii
orally for 7 weeks.
Results
The arthritis score and joint tissue damage were decreased in the mice administered
F. prausnitzii
compared with the vehicle-treated group. In addition, administration of
F. prausnitzii
reduced the abundance of systemic immune cells that secrete the pro-inflammatory cytokine IL-17 and induced changes in SCFA concentrations and the intestinal microbial flora composition. It also resulted in decreased lactate and acetate concentrations, an increased butyrate concentration, and altered compositions of bacteria known to exacerbate or improve RA.
Conclusion
These results suggest that
F. prausnitzii
exerts a therapeutic effect on RA by regulation of IL-17 producing cells. In addition,
F. prausnitzii
modify the microbial flora composition and short chain fatty acids in experimental RA mouse model.
Journal Article
IL-17 Induces Autophagy Dysfunction to Promote Inflammatory Cell Death and Fibrosis in Keloid Fibroblasts via the STAT3 and HIF-1α Dependent Signaling Pathways
Keloid is an abnormal fibrotic disease after cutaneous injury characterized by exaggerated scar tissue formation, which often extends beyond the boundaries of the original wound. Although chronic inflammation is known to be associated with the excessive inflammation in keloid tissue, there are few studies on the role of autophagy in the pathogenesis of keloid. In this study, we evaluated the pattern of autophagy in keloid fibroblasts (KF) and normal fibroblasts (NF). Expression of HIF-1α, STAT3 and autophagic flux markers were evaluated in KF and NF. Defective autophagy caused by IL-17 was evaluated, and the relationship between defective autophagy and necroptosis was also examined. The expression of IL-17, HIF-1α and STAT3 was significantly increased in keloid tissue, and autophagosome-to autophagolysosome conversion was defective in KF. IL-17 treatment significantly elevated the expression of STAT3 and HIF-1α in NF and caused defective autophagy, which was reversed by HIF-1α inhibitor. In addition, the defective autophagy was associated with the increased necroptosis and fibrosis. In keloid tissue, the elevated necroptosis marker was confirmed, and with the HIF-1α inhibitor, the defective autophagy, necroptosis and fibrosis was decreased in KF. In conclusion, autophagy was defective in keloid tissue, which was associated with increased necroptosis and fibrosis. The IL-17-STAT3-HIF-1α axis was involved in defective autophagy in KF, and this suggests that targeting the axis could alleviate chronic inflammation in keloid disease.
Journal Article
Genetics of Aldosterone-Producing Adenoma in Korean Patients
Recently, somatic mutations in KCNJ5, ATP1A1, ATP2B3, and CACNA1D genes were found to be associated with the pathogenesis of aldosterone-producing adenoma (APA). This study aimed to investigate the prevalence of somatic mutations in KCNJ5, ATP1A1, ATP2B3, and CACNA1D and examine the correlations between these mutations and the clinical and biochemical characteristics in Korean patients with APA.
We performed targeted gene sequencing in 66 patients with APA to detect somatic mutations in these genes.
Somatic KCNJ5 mutations were found in 47 (71.2%) of the 66 patients with APA (31 cases of p.G151R and 16 cases of p.L168R); these two mutations were mutually exclusive. Somatic mutations in the ATP1A1, ATP2B3, and CACNA1D genes were not observed. Somatic KCNJ5 mutations were more prevalent in female patients (66% versus 36.8%, respectively; P = 0.030). Moreover, patients with KCNJ5 mutations comprised a significantly higher proportion of patients younger than 35 years of age (19.1% versus 0%, respectively; P = 0.040). There were no significant differences in pre-operative blood pressure, plasma aldosterone, serum potassium, lateralization index, and adenoma size according to mutational status. Patients with KCNJ5 mutations were less likely to need antihypertensive medications after adrenalectomy compared with those without mutation (36.2% versus 63.2%; P = 0.045).
The present study demonstrated the high prevalence of somatic KCNJ5 mutations in Korean patients with APA. Carriers of somatic KCNJ5 mutations were more likely to be female. Early diagnosis and better therapeutic outcomes were associated with somatic KCNJ5 mutations in APA.
Journal Article
Adiponectin and 8-epi-PGF2α as intermediate influencing factors in weight reduction after legume consumption: a 12-week randomised controlled trial
Legumes are rich sources of essential nutrients, and their potential health benefits were reported in many studies. Several studies showed a positive effect of legumes on obesity, but randomised clinical trials are limited in the Korean population. The present intervention study investigated the impact of legumes on body weight in obese Korean subjects. A total of 400 participants (BMI ≥ 25 kg/m2) were randomised into two groups. The legume-enriched diet (LD) group replaced one-third of their refined rice consumption with legumes three times per day as a carbohydrate source. In contrast, the usual diet (UD) group consumed their UD. The mean weight loss at 12 weeks was 2·87 (sem 0·21) kg and 0·17 (sem 0·11) kg in the LD and UD, respectively, which was significantly different between the groups (P < 0·001). HDL-cholesterol and adiponectin levels were increased, and levels of glucose, insulin, TAG, and 8-epi-PGF2α and the homoeostasis model assessment of insulin resistance (IR) index value decreased at 12 weeks compared with baseline in the LD. The consumption of legumes may accelerate weight loss accompanied by regulation of adiponectin and 8-epi-PGF2α in obese subjects. In particular, legumes seemed to induce significant changes in BMI by increasing adiponectin in females. Additionally, increases in plasma adiponectin due to greater substantial weight loss may be related to the improvement in IR.
Journal Article