Ion channels are highly diverse in the cnidarian model organism Nematostella vectensis (Anthozoa), but little is known about the evolutionary origins of this channel diversity and its conservation across Cnidaria. Here we examined the evolution of voltage-gated K+ channels in Cnidaria by comparing genomes and transcriptomes of diverse cnidarian species from Anthozoa and Medusozoa. We found an average of over 40 voltage-gated K+ channel genes per species, and phylogenetic reconstruction of the Kv, KCNQ and EAG gene families identified 28 voltage-gated K+ channels present in the last common ancestor of Anthozoa and Medusozoa (23 Kv, 1 KCNQ and 4 EAG). Thus, much of the diversification of these channels took place in the stem cnidarian lineage prior to the emergence of modern cnidarian classes. In contrast, the stem bilaterian lineage, from which humans evolved, contained no more than 9 voltage-gated K+ channels. These results hint at a complexity to electrical signaling in all cnidarians that contrasts with the perceived anatomical simplicity of their neuromuscular systems. These data provide a foundation from which the function of these cnidarian channels can be investigated, which will undoubtedly provide important insights into cnidarian physiology.
BackgroundFibromyalgia (FM) is a widespread chronic disease characterized by chronic pain and fatigue that has a strong impact on the quality of life of patients, who represent the 6% of the world population. There is no molecular analysis FM condition, being currently diagnosed through clinical self-questionnaires. Since FM patients present a strong lack of energy and several gastrointestinal disturbances, the relationship between the microbiota-mitochondrial axis could be a relevant mechanism [1]. The intestinal microbiota has a great impact on health and energy balances. When the distribution is altered, intestinal dysbiosis appears and the majority of the dysbiosis-related conditions are strongly related to FM [2]. As a result, some authors have pointed to the intestinal microbiota as the main player in FM [3]. The intestinal microbiota works as an intermediary in the final goal of provide energy to cells through the production of ATP, the core task of mitochondria. This organelle is especially abundant in tissues such as muscle and brain, both affected by the etiology of FM [4]. In addition, many studies have highlighted the involvement of mitochondrial imbalances and oxidative stress in patients with FM [5]. Interestingly, crosstalk between mitochondria and microbiota is implicated in inflammation [6], a hallmark of FM.ObjectivesTo characterize intestinal microbiota composition and mitochondrial balance in a cohort of FM patients.MethodsA group of 26 patients (7 men and 19 women) diagnosed with primary FM according to the ACR criteria where selected. Intestinal microbiota composition was determined by qPCR of some central genera as well as secretory IgA levels. Mitochondrial mass was determined by western blot in peripheral blood mononuclear cells protein (PBMC) to detect mitochondrial mass and mitophagy biomarkers. Additionally, Total Antioxidant Capacity (TAC) was measured with e-BQC lab (Bioquochem, Asturias, Spain), an electronic device that oxidizes the samples by applying an electrochemical current.ResultsRoseburiaspp./Eubacteriumspp. ratio is shifted toRoseburiaspecies, andAkkermansia muciniphilahas lost its representativeness. Additionally, more than half of the patients presented sIgA values below the reference range. Lastly, the mitochondrial ratio showed a mitochondrial imbalance in most of the patients, which had higher mitochondrial mass.ConclusionThe results suggested an imbalanced intestinal microbiota and mitochondrial ratio in FM. These results open up a wide range of possibilities, both to develop treatments and diagnostic techniques for the disease.References[1]Jung, Y.H.; Kim, H.; Lee, D.; Lee, J.Y.; Moon, J.Y.; Choi, S.H.; Kang, D.H. Dysfunctional Energy Metabolisms in Fibromyalgia Compared with Healthy Subjects. Mol Pain 2021, 17[2]Collado, A.; Gomez, E.; Coscolla, R.; Sunyol, R.; Solé, E.; Rivera, J.; Altarriba, E.; Carbonell, J.; Castells, X. Work, Family and Social Environment in Patients with Fibromyalgia in Spain: An Epidemiological Study: EPIFFAC Study. BMC Health Serv Res 2014, 14,[3]Clos-Garcia, M.; Andrés-Marin, N.; Fernández-Eulate, G.; Abecia, L.; Lavín, J.L.; van Liempd, S.; Cabrera, D.; Royo, F.; Valero, A.; Errazquin, N.; et al. Gut Microbiome and Serum Metabolome Analyses Identify Molecular Biomarkers and Altered Glutamate Metabolism in Fibromyalgia. EBioMedicine 2019, 46, 499–511[4]Siracusa, R.; di Paola, R.; Cuzzocrea, S.; Impellizzeri, D. Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update. International Journal of Molecular Sciences 2021, Vol. 22, Page 3891 2021, 22, 3891[5]Sánchez-Domínguez, B.; Bullón, P.; Román-Malo, L.; Marín-Aguilar, F.; Alcocer-Gómez, E.; Carrión, A.M.; Sánchez-Alcazar, J.A.; Cordero, M.D. Oxidative Stress, Mitochondrial Dysfunction and, Inflammation Common Events in Skin of Patients with Fibromyalgia. Mitochondrion 2015, 21, 69–75[6]Jackson, D.N.; Theiss, A.L. Gut Bacteria Signaling to Mitochondria in Intestinal Inflammation and Cancer. Gut Microbes 2020, 11, 285–304Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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