PCNA and apoptosis during post-spawning ovarian remodeling in the teleost Oreochromis niloticus

Martins

et al. 2019

Zygote

Self Cite

SummaryThe present study evaluated the effects of low salinity on the early larval development of Oreochromis niloticus, specifically histological damage to white muscle, morphology of the yolk-sac surface and trunk area, and molecular expression of apoptosis and cell proliferation biomarkers. Newly hatched larvae were submitted to four salinity treatments for a period of 48 or 72 h, in duplicate: (S0) freshwater, (S2) 2 g l−1, (S4) 4 g l−1, and (S6) 6 g l−1NaCl. Larval development was examined using histology, electron microscopy, enzyme-linked immunosorbent assay (ELISA), and morphometry. At the yolk-sac surface, larvae of S4 and S6 displayed alterations to the apical opening of chloride cells that may be related to osmotic expenditure caused by the increased salinity. Caspase-3 expression did not differ significantly among treatments, however significantly lower proliferating cell nuclear antigen (PCNA) expression (P < 0.05) suggested minor cell proliferation in larvae of S4 and S6 compared with S0 and S2. Furthermore, there was a significant reduction in both trunk area and percentage of normal white muscle fibres (WF) in larvae of S4 and S6. Vacuolated areas and myofibrils concentrated at the cell periphery and found in the white muscle from larvae exposed to saline environments suggested disturbance to muscle development. Oedema and mononuclear infiltrate were also observed in the white muscle of S4 and S6 larvae. Together these results indicated that treatments with 4 and 6 g l−1 NaCl may cause osmoregulation expenditure, morphological alterations to the yolk-sac surface and histological damage to skeletal muscle that negatively affected the early larval development of O. niloticus.

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 56%

Low salinity negatively affects early larval development of Nile tilapia, Oreochromis niloticus: insights from skeletal muscle and molecular biomarkers

Martins

et al. 2019

Zygote

Self Cite

“…The present study revealed that IRI induced a number of pathological, functional and molecular changes in the liver, including increased serum levels of ALT and AST, the downregulation of miR-101, mTOR mRNA and p62, increased levels of LC3II and caspase-3, decreased intra-nuclear PCNA and extensive tissue necrosis and apoptosis. PCNA is closely associated with cellular DNA synthesis and therefore a good indicator of cell proliferation status (51,52). Caspase-3 is a necessary terminal cleavage enzyme in the intrinsic apoptotic pathway, and an established indicator of apoptosis (53).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-101 inhibits autophagy to alleviate liver ischemia/reperfusion injury via regulating the mTOR signaling pathway

Wang

et al. 2019

Int J Mol Med

Liver ischemia/reperfusion injury (LIRI) is a common complication of liver surgery, and affects liver function post-transplantation. However, the precise mechanism underlying LIRI has not yet been completely elucidated. Previous studies have demonstrated the involvement of a number of microRNAs (miRNAs/miRs) in liver pathophysiology. The objective of the present study was to determine the potential function and mechanism of miR-101-mediated regulation of autophagy in LIRI. Compared with the sham-treated group, a significant decrease in miR-101 and mechanistic target of rapamycin (mTOR) expression levels following ischemia/reperfusion (IR) were observed, along with an increased number of autophagosomes (P<0.001). The exogenous overexpression of miR-101 has been demonstrated to inhibit autophagy during the LIRI response and the levels of mTOR and phosphorylated (p)-mTOR expression are correspondingly elevated. However, compared with the miR-NC group, miR-101 silencing was associated with reduced mTOR and p-mTOR levels and increased autophagy, as indicated by the gradual increase in the levels of the microtubule-associated protein 1 light II (LC3II). The peak levels of LC3II were observed 12 h subsequent to reperfusion, which coincided with the lowest levels of miR-101. In addition, inhibition of autophagy by 3-methyladenine significant enhanced the protective effect of miR-101 against LIRI, compared with the IR group (P<0.001). Altogether, miR-101 attenuates LIRI by inhibiting autophagy via activating the mTOR pathway.

“…As well as in other teleost species, follicular atresia in Nile tilapia occurs during follicular growth but is more frequent in vitellogenic follicles that were not spawned in the reproductive season (Miranda, Bazzoli, Rizzo, & Sato, ; Santos et al, ). In this species, the follicular atresia is a good model to study the cell death pathways since females breed every three to 4 weeks under optimum cultivation conditions, and atretic follicles (AF) are present throughout the reproductive cycle (Melo, Martins, Luz, Rizzo, & Bazzoli, ; Melo et al, ). To improve the knowledge of cell death mechanisms regulating follicular atresia, we investigated the expression, interaction, and dynamics existing between key proteins of autophagy and apoptosis pathways and the crosstalk with lysosomal proteins in different phases of follicular atresia in Nile tilapia.…”

Section: Introductionmentioning

confidence: 99%

Autophagy and Cathepsin D mediated apoptosis contributing to ovarian follicular atresia in the Nile tilapia

Sales

Molecular Reproduction Devel

Pinheiro

et al. 2019

Self Cite

Follicular atresia is a hormonally controlled degenerative process involving apoptosis of the somatic and germ cells. Since different signaling pathways can induce cell death, the aim of the present study was to investigate cell death signaling and crosstalk between autophagic, apoptotic, and lysosomal proteins during follicular atresia in Nile tilapia. For this, females were kept in controlled conditions for 21 days, and ovary samples were collected weekly. The atretic follicles (AF) were analyzed in three regression phases: Early, advanced, and late. Under electron microscopy, the follicular cells exhibited numerous protein synthesis organelles in the early AF. Immunoreactivity for Bcl2, Beclin1, Lc3, and Cathepsin D increased significantly in advanced AF (p < .001), when follicular cells were in intense yolk phagocytosis. In this phase, autophagosomes and autolysosomes were frequently observed. In the late AF, follicular cells had a markedly electron‐lucid cytoplasm and immunoreactivity for Bax and TUNEL assay indicated an elevated apoptosis rate. Colocalisation of Lamp1/Cathepsin D and Lc3/Caspase‐3 suggests dynamic crosstalk between the autophagy, apoptosis, and lysosome pathways. Taken together, the data indicate that autophagy plays a role in the homeostasis and clearance of the follicular cells preceding Cathepsin D mediated apoptosis during follicular atresia in Nile tilapia.