Coding and Noncoding Genes Involved in Atrophy and Compensatory Muscle Growth in Nile Tilapia.

Improvements in growth-related traits reduce fish time and production costs to reach market size. Feed deprivation and refeeding cycles have been introduced to maximize aquaculture profits through compensatory growth. However, the molecular compensatory growth signature is still uncertain in Nile tilapia. In this study, fish were subjected to two weeks of fasting followed by two weeks of refeeding. The growth curve in refed tilapia was suggestive of a partial compensatory response. Transcriptome profiling of starved and refed fish was conducted to identify genes regulating muscle atrophy and compensatory growth. Pairwise comparisons revealed 5009 and 478 differentially expressed (differential) transcripts during muscle atrophy and recovery, respectively. Muscle atrophy appears to be mediated by the ubiquitin-proteasome and autophagy/lysosome systems. Autophagy-related 2A, F-box and WD repeat domain containing 7, F-box only protein 32, miR-137, and miR-153 showed exceptional high expression suggesting them as master regulators of muscle atrophy. On the other hand, the muscle compensatory growth response appears to be mediated by the continuous stimulation of muscle hypertrophy which exceeded normal levels found in control fish. For instance, genes promoting ribosome biogenesis or enhancing the efficiency of translational machinery were upregulated in compensatory muscle growth. Additionally, myogenic microRNAs (e.g., miR-1 and miR-206), and hypertrophy-associated microRNAs (e.g., miR-27a-3p, miR-29c, and miR-29c) were reciprocally expressed to favor hypertrophy during muscle recovery. Overall, the present study provided insights into the molecular mechanisms regulating muscle mass in fish. The study pinpoints extensive growth-related gene networks that could be used to inform breeding programs and also serve as valuable genomic resources for future mechanistic studies.

Therapeutic effects of mesenchymal stem cells and vitamin D on Bleomycin triggered lung damage in male adult albino rats.

Bleomycin is a cancer chemotherapeutic agent that induces pulmonary fibrosis. Vitamin D plays an immunomodulation role. Bone marrow-derived mesenchymal stem cells have a strong therapeutic effect in fatal pulmonary fibrosis. The objective of this study was to evaluate the significance of vitamin D and bone marrow mesenchymal stem cells as therapeutic agents on lung injuries caused by Bleomycin in adult male rats. Thirty-five adult male albino rats were allocated into five experimental groups. The control group was the group I. The group given a single intratracheal instillation of Bleomycin was group II. The group was given vitamin D3 for 2 days before Bleomycin administration was group III. Group IV was the group that was injected by a single dose of mesenchymal stem cells (MSCs) after 4 weeks of Bleomycin injection. Group V was the withdrawal group. Histological, immunohistochemical, and ultrastructural techniques were used to process and evaluate lung tissues. The lung of group 2 was demonstrated interalveolar septal thickening by RBCs, infiltration of mononuclear cells, deposition of collagen, and marked positive alpha-smooth muscle actin immunoreactivity. Mesenchymal stem cells derived from bone marrow can diminish Bleomycin-generated fibrosis of the lungs and inflammation in rats better than vitamin D treatment.

Expressions and characterization of MuRFs, Atrogin-1, F-box25 genes in tilapia, Oreochromis niloticus, in response to starvation.

Muscle accretion is affected by the difference between protein synthesis and its degradation. Studies on different species revealed that muscle proteolysis is mediated by different pathways including the ubiquitin-proteasome pathway in which the ubiquitin protein ligases play an important role. These muscle atrophy associated ligases were not well studied in tilapia. In this study, we characterized the ubiquitin protein ligases MuRF1/2/3, Atrogin-1 and F-box25, members of the ubiquitin-proteasome pathway in tilapia, Oreochromis niloticus, and their expressions in the muscle of starved, fed, refed, and control fish. Sequences of these genes revealed presence of Ring finger, B-box, and Cos domains in all MuRF genes, as well as F-box domain in Atrogin-1 and F-box25 genes. Real-time qPCR data analysis showed that expression of MuRF1/2/3, Atrogin-1, F-box25, and proteasome complex genes was significantly upregulated in starved fish compared to fed fish. Concurrently, the proteasome activity was 1.7-folds elevated in the starved fish compared to fed fish. These results confirm the important role of these genes in muscle degradation and suggest potential usage as markers of muscle accretion in tilapia.