Grass carp prolactin: Molecular cloning, tissue expression, intrapituitary autoregulation by prolactin and paracrine regulation by growth hormone and luteinizing hormone

Lin, Cheng Yuan; Jiang, Xiyi; Hu, Guangfu; Ko, Wendy K. W.; Wong, Anderson O. L.

doi:10.1016/j.mce.2014.10.010

Cited by 25 publications

(23 citation statements)

References 73 publications

(115 reference statements)

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“…The authenticity of PCR products (947 bp and 911 bp for activin βA and βB, respectively) was routinely confirmed by PCR Southern using DIG-labelled probes for the respective gene targets. To characterize the size and form(s) of activin β transcripts expressed at the pituitary level, total RNA prepared from the carp pituitary was size-fractionated in 1% agarose gel and subjected to Northern blot using DIG-labelled riboprobes for carp activin βA and βB as described previously [37]. To test if the two activin β isoforms are expressed in a cell type-specific manner at the pituitary level, RT-PCR coupled with laser capture microdissection (LCM) of immuno-identified somatotrophs (GH cells), lactotrophs (PRL cells) and gonadotrophs (LH cells) was also performed.…”

Section: Methodsmentioning

confidence: 99%

“…In grass carp pituitary cells, autoregulation of GH [36] as well as other members of GH gene lineage including prolactin (PRL, [37]) and somatolactin [38] have been reported. In the carp pituitary, local release of GH was shown to induce PRL release and gene expression and these paracrine effects of GH could be inhibited by local release of LH [37]. In the same animal model, an intrapituitary feedback loop for GH regulation via autocrine/paracrine interaction of goandotrophs and somatotrophs has been reported [39].…”

Section: Introductionmentioning

confidence: 99%

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Activin/follistatin system in grass carp pituitary cells: - Regulation by local release of growth hormone and luteinizing hormone and its functional role in growth hormone synthesis and secretion

et al. 2017

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Gonadotrophin regulation by activin/follistatin system is well-documented, but the corresponding effect on growth hormone (GH) has not been fully characterized and with little information available in lower vertebrates, especially in fish models. In grass carp, local interactions of GH and luteinizing hormone (LH) can induce GH release and gene expression at pituitary level via autocrine/paracrine mechanisms. To shed light on the role of activin/follistatin system in GH regulation by local actions of GH and LH, grass carp activin βA and βB were cloned, shown to be single-copy genes expressed in the pituitary, and confirmed to encode activin proteins capable of transactivating promoter with activin-responsive elements. In grass carp pituitary cells, activin A and B were effective in reducing GH secretion and GH cell content with concurrent drop in GH mRNA level whereas the opposite was true for follistatin, the activin-binding protein known to neutralize the effects of endogenous activin. Treatment with activin A and B not only could suppress basal but also inhibit GH mRNA expression induced by GH and human chorionic gonadotropin (hCG), a functional analogue of LH in fish model. Apparently, down-regulation of GH mRNA by activin was mediated by reducing GH transcript stability with concurrent inhibition on GH promoter activity via the SMAD pathway. In reciprocal experiments, GH treatment was found to up-regulate activin βA, activin βB and follistatin mRNA levels in carp pituitary cells but the opposite was noted by removing endogenous GH with GH antiserum. Interestingly, parallel treatment with hCG could also inhibit basal as well as GH-induced activin βA, activin βB and follistatin gene expression. These results, as a whole, indicate that the pituitary activin/follistatin system can serve as a regulatory target for local interactions of GH and LH and contribute to GH regulation by autocrine/paracrine mechanisms in the carp pituitary.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activin/follistatin system in grass carp pituitary cells: - Regulation by local release of growth hormone and luteinizing hormone and its functional role in growth hormone synthesis and secretion

et al. 2017

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“…Sequence alignment, 3D protein modeling, and phylogenetic analysis were conducted using CLUSTAL-W, SWISS-MODEL, and MEGA 6.0 respectively. To deduce gene copy number of Socs1-3 and Cish, Southern blot was performed in genomic DNA isolated from carp blood (Lin et al 2015). For tissue expression of type II SOCS, northern blot was conducted in total RNA prepared from the carp liver and pituitary, whereas RT-PCR was examined in selected tissues/brain areas using primers for respective gene targets with PCR conditions described in Table 1.…”

Section: Molecular Cloning Copy Number and Tissue Expression Of Socmentioning

confidence: 99%

Type II SOCS as a feedback repressor for GH-induced Igf1 expression in carp hepatocytes

Jiang

Jia

et al. 2016

Journal of Endocrinology

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Type II suppressor of cytokine signaling (SOCS) serve as feedback repressors for cytokines and are known to inhibit growth hormone (GH) actions. However, direct evidence for SOCS modulation of GH-induced insulin-like growth factor 1 (Igf1) expression is lacking, and the post-receptor signaling for SOCS expression at the hepatic level is still unclear. To shed light on the comparative aspects of SOCS in GH functions, grass carp was used as a model to study the role of type II SOCS in GH-induced Igf1 expression. Structural identity of type II SOCS, Socs1-3 and cytokine-inducible SH2-containing protein (Cish), was established in grass carp by 5'/3'-RACE, and their expression at both transcript and protein levels were confirmed in the liver by RT-PCR and LC/MS/MS respectively. In carp hepatocytes, GH treatment induced rapid phosphorylation of JAK 2 , STATs, MAPK, PI3K, and protein kinase B (Akt) with parallel rises in socs1-3 and cish mRNA levels, and these stimulatory effects on type II SOCS were shown to occur before the gradual loss of igf1 gene expression caused by prolonged exposure of GH. Furthermore, GH-induced type II SOCS gene expression could be negated by inhibiting JAK 2 , STATs, MEK 1/2 , P 38 MAPK , PI3K, and/or Akt respectively. In CHO cells transfected with carp GH receptor, over-expression of these newly cloned type II SOCS not only suppressed JAK 2 /STAT 5 signaling with GH treatment but also inhibited GH-induced grass carp Igf1 promoter activity. These results, taken together, suggest that type II SOCS could be induced by GH in the carp liver via JAK 2 /STATs, MAPK, and PI3K/Akt cascades and serve as feedback repressors for GH signaling and induction of igf1 gene expression.

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“…The cell pellets were then dissolved in mitochondria extraction buffer mix and vortex for 10 s to obtain the mitochondrial fraction. Western blot analysis was conducted as described previously (Lin et al, 2015). Protein concentration was detected using Pierce BCA protein assay kit (Thermo Fisher Scientific Inc, MA, United States), subjected to 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to polyvinylidene difluoride membranes.…”

Section: Methodsmentioning

confidence: 99%

Azoxystrobin Induces Apoptosis of Human Esophageal Squamous Cell Carcinoma KYSE-150 Cells through Triggering of the Mitochondrial Pathway

et al. 2017

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Recent studies indicate that mitochondrial pathways of apoptosis are potential chemotherapeutic target for the treatment of esophageal cancer. Azoxystrobin (AZOX), a methoxyacrylate derived from the naturally occurring strobilurins, is a known fungicide acting as a ubiquinol oxidation (Qo) inhibitor of mitochondrial respiratory complex III. In this study, the effects of AZOX on human esophageal squamous cell carcinoma KYSE-150 cells were examined and the underlying mechanisms were investigated. AZOX exhibited inhibitory effects on the proliferation of KYSE-150 cells with inhibitory concentration 50% (IC50) of 2.42 μg/ml by 48 h treatment. Flow cytometry assessment revealed that the inhibitory effect of AZOX on KYSE-150 cell proliferation occurred with cell cycle arrest at S phase and increased cell apoptosis in time-dependent and dose-dependent manners. Cleaved poly ADP ribose polymerase (PARP), caspase-3 and caspase-9 were increased significantly by AZOX. It is worth noted that the Bcl-2/Bax ratios were decreased because of the down-regulated Bcl-2 and up-regulated Bax expression level. Meanwhile, the cytochrome c release was increased by AZOX in KYSE-150 cells. AZOX-induced cytochrome c expression and caspase-3 activation was significantly blocked by Bax Channel Blocker. Intragastric administration of AZOX effectively decreased the tumor size generated by subcutaneous inoculation of KYSE-150 cells in nude mice. Consistently, decreased Bcl-2 expression, increased cytochrome c and PARP level, and activated caspase-3 and caspase-9 were observed in the tumor samples. These results indicate that AZOX can effectively induce esophageal cancer cell apoptosis through the mitochondrial pathways of apoptosis, suggesting AZOX or its derivatives may be developed as potential chemotherapeutic agents for the treatment of esophageal cancer.

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Grass carp prolactin: Molecular cloning, tissue expression, intrapituitary autoregulation by prolactin and paracrine regulation by growth hormone and luteinizing hormone

Cited by 25 publications

References 73 publications

Activin/follistatin system in grass carp pituitary cells: - Regulation by local release of growth hormone and luteinizing hormone and its functional role in growth hormone synthesis and secretion

Activin/follistatin system in grass carp pituitary cells: - Regulation by local release of growth hormone and luteinizing hormone and its functional role in growth hormone synthesis and secretion

Type II SOCS as a feedback repressor for GH-induced Igf1 expression in carp hepatocytes

Azoxystrobin Induces Apoptosis of Human Esophageal Squamous Cell Carcinoma KYSE-150 Cells through Triggering of the Mitochondrial Pathway

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