Myostatin-mediated regulation of skeletal muscle damage post-acute Aeromonas hydrophila infection in Nile tilapia (Oreochromis niloticus L.).

This study focuses on the relationship between myostatin (MyoS), myogenin (MyoG), and the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis for muscle growth and histopathological changes in muscle after an Aeromonas hydrophila infection. A total number of 90 Nile tilapia (55.85 g) were randomly allocated into two equal groups of three replicates each. The first group was an uninfected control group that was injected intraperitoneally (ip) with 0.2 ml phosphate buffer saline (PBS), while the second group was injected ip with 0.2 ml (1.3 × 108 CFU/ml) Aeromonas hydrophila culture suspension. Sections of white muscle and liver tissues were taken from each group 24 h, 48 h, 72 h, and 1 week after infection for molecular analysis and histopathological examination. The results revealed that with time progression, the severity of muscle lesions increased from edema between bundles and mononuclear inflammatory cell infiltration 24 h post-challenge to severe atrophy of muscle bundles with irregular and curved fibers with hyalinosis of the fibers 1 week postinfection. The molecular analysis showed that bacterial infection was able to induce the muscle expression levels of GH with reduced ILGF-1, MyoS, and MyoG at 24 h postinfection. However, time progression postinfection reversed these findings through elevated muscle expression levels of MyoS with regressed expression levels of muscle GH, ILGF-1, and MyoG. There have been no previous reports on the molecular expression analysis of the aforementioned genes and muscle histopathological changes in Nile tilapia following acute Aeromonas hydrophila infection. Our findings, collectively, revealed that the up-and down-regulation of the myostatin signaling is likely to be involved in the postinfection-induced muscle wasting through the negative regulation of genes involved in muscle growth, such as GH, ILGF-1, and myogenin, in response to acute Aeromonas hydrophila infection in Nile tilapia, Oreochromis niloticus.

Exploring the impacts of different fasting and refeeding regimes on Nile tilapia (Oreochromis niloticus L.): growth performance, histopathological study, and expression levels of some muscle growth-related genes.

The current study investigated how different fasting and refeeding regimes would impact Nile tilapia growth performance, histopathological examination, and gene expression of myostatin, myogenin, GH, IGF-1, and NPYa. Nile tilapia fish (n = 120) were randomly allocated into four groups, including the control group fed on a basal diet for 6 weeks (F6), group A starved for 1 week and then refed for 5 weeks (S1F5), group B starved for 2 weeks and then refed for 4 weeks (S2F4), while group C starved for 4 weeks and then refed for 2 weeks (S4F2). Fasting provoked a decrease in body weight coincided with more extended starvation periods. Also, it induced muscle and liver histological alterations; the severity was correlated with the length of fasting periods. Gene expression levels of GH, MSTN, MYOG, and NPYa were significantly increased, while IGF1 was markedly depressed in fasted fish compared to the control group. Interestingly, refeeding after well-planned short fasting period (S1F5) modulated the histopathological alterations. To some extent, these changes were restored after refeeding. Restored IGF-I and opposing fasting expression profiles of the genes mentioned above thus recovered weights almost like the control group and achieved satisfactory growth compensation. Conversely, refeeding following more extended fasting periods failed to restore body weight. In conclusion, refeeding after fasting can induce a compensatory response. Still, the restoration capacity is dependent on the length of fasting and refeeding periods through exhibiting differential morphological structure and expressions pattern for muscle and growth-related genes.

Collagen extract obtained from Nile tilapia (Oreochromis niloticus L.) skin accelerates wound healing in rat model via up regulating VEGF, bFGF, and α-SMA genes expression.

BACKGROUND: Collagen is the most abundant structural protein in the mammalian connective tissue and represents approximately 30% of animal protein. The current study evaluated the potential capacity of collagen extract derived from Nile tilapia skin in improving the cutaneous wound healing in rats and investigated the underlying possible mechanisms. A rat model was used, and the experimental design included a control group (CG) and the tilapia collagen treated group (TCG). Full-thickness wounds were conducted on the back of all the rats under general anesthesia, then the tilapia collagen extract was applied topically on the wound area of TCG. Wound areas of the two experimental groups were measured on days 0, 3, 6, 9, 12, and 15 post-wounding. The stages of the wound granulation tissues were detected by histopathologic examination and the expression of vascular endothelial growth factor (VEGF), and transforming growth factor (TGF-ß1) were investigated using immunohistochemistry. Moreover, relative gene expression analysis of transforming growth factor-beta (TGF-ß1), basic fibroblast growth factor (bFGF), and alpha-smooth muscle actin (α-SMA) were quantified by real-time qPCR. RESULTS: The histopathological assessment showed noticeable signs of skin healing in TCG compared to CG. Immunohistochemistry results revealed remarkable enhancement in the expression levels of VEGF and TGF-ß1 in TCG. Furthermore, TCG exhibited marked upregulation in the VEGF, bFGF, and α-SMA genes expression. These findings suggested that the topical application of Nile tilapia collagen extract can promote the cutaneous wound healing process in rats, which could be attributed to its stimulating effect on recruiting and activating macrophages to produce chemotactic growth factors, fibroblast proliferation, and angiogenesis. CONCLUSIONS: The collagen extract could, therefore, be a potential biomaterial for cutaneous wound healing therapeutics.