Proliferation and mRNA expression of absorptive villous cell markers and mineral transporters in prolactin‐exposed IEC‐6 intestinal crypt cells

Teerapornpuntakit, Jarinthorn; Wongdee, Kannikar; Thongbunchoo, Jirawan; Krishnamra, Nateetip; Charoenphandhu, Narattaphol

doi:10.1002/cbf.2807

Cited by 9 publications

(3 citation statements)

References 36 publications

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“…Claudin-15, which regulates the epithelial cation selectivity and paracellular Ca 2+ movement, is required for this PRL-enhanced paracellular transport 145 . PRL is found to downregulate the expression of claudin-3 and occludin in IEC-6 crypt cells, a rat small intestine epithelial cell line 146 . Cofilin is an actin binding protein and its dephosphorylation corresponds to the TJ opening, TER decrease and claudin-1 dissociation from the cytoskeleton.…”

Section: Disruptions Of Claudin-mediated Intestinal Barriersmentioning

confidence: 98%

Claudins in intestines

et al. 2013

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Intestines are organs that not only digest food and absorb nutrients, but also provide a defense barrier against pathogens and noxious agents ingested. Tight junctions (TJs) are the most apical component of the junctional complex, providing one form of cell-cell adhesion in enterocytes and playing a critical role in regulating paracellular barrier permeability. Alteration of TJs leads to a number of pathophysiological diseases causing malabsorption of nutrition and intestinal structure disruption, which may even contribute to systemic organ failure. Claudins are the major structural and functional components of TJs with at least 24 members in mammals. Claudins have distinct charge-selectivity, either by tightening the paracellular pathway or functioning as paracellular channels, regulating ions and small molecules passing through the paracellular pathway. In this review, we have discussed the functions of claudin family members, their distribution and localization in the intestinal tract of mammals, their alterations in intestine-related diseases, and chemicals/agents that regulate the expression and localization of claudins as well as the intestinal permeability, which provide a therapeutic view for treating intestinal diseases.

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Section: Disruptions Of Claudin-mediated Intestinal Barriersmentioning

confidence: 98%

Claudins in intestines

et al. 2013

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“…In adult rats, PRL induces active potassium-ion transport in distal colon and chloride-ion transport in proximal and transverse colon (21). IEC-6 colon crypt epithelial cells treated with PRL had increased expression of nutrient and mineral transport channel proteins, without inducing proliferation (22). Elevated serum levels of PRL have been identified in patients with colorectal malignancies (23)(24)(25)(26).…”

Section: Introductionmentioning

confidence: 99%

Prolactin signaling enhances colon cancer stemness by modulating Notch signaling in a Jak2-STAT3/ERK manner

Neradugomma¹,

Subramaniam²,

Tawfik³

et al. 2013

Carcinogenesis

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Prolactin (PRL) is a secretory cytokine produced by various tissues. Binding to the cognate PRL receptor (PRLR), it activates intracellular signaling via janus kinase (JAK), extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription (STAT) proteins. PRL regulates diverse activities under normal and abnormal conditions, including malignancies. Previous clinical data suggest serum PRL levels are elevated in colorectal cancer (CRC) patients. In this study, we first determined the expression of PRL and PRLR in colon cancer tissue and cell lines. Higher levels of PRLR expression were observed in the cancer cells and cell lines compared with normal colonic epithelial cells. Incubation of colon cancer cells with PRL-induced JAK2, STAT3 and ERK1/2 phosphorylation and increased expression of Jagged 1, which is a Notch-1 receptor ligand. Notch signaling regulates CRC stem cell population. We observed increased accumulation of the cleaved/active form of Notch-1 receptor (Notch intracellular domain) and increased expression of Notch responsive genes HEY1, HES1 and stem cell marker genes DCLK1, LGR5, ALDH1 and CD44. Finally, inhibiting PRL induced JAK2-STAT3 and JAK2-ERK1/2 using AG490 and PD98059, respectively, leads to complete abrogation of Notch signaling, suggesting a role for this pathway in regulating CRC stem cells. Together, our results demonstrate that cytokine signaling induced by PRL is active in colorectal cancers and may provide a novel target for therapeutic intervention.

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“…Recent research has demonstrated multiple roles for PRL in the small intestine of mammals. In rodents, PRL mediates water uptake and retention during lactation in addition to the uptake of glucose, sodium, chloride and amino acids to support fluid, solute and energy requirements (Ramsey & Bern 1972, Mainoya 1975, Teerapornpuntakit et al 2012. Both active and passive transport mechanisms of calcium uptake are rapidly stimulated by PRL via the phosphoinositide 3-kinase pathway (Jantarajit et al 2007, Ryszka et al 2012.…”

Section: Figure 11mentioning

confidence: 99%

Comparative genomics reveals tissue-specific regulation of prolactin receptor gene expression

Schennink¹,

Trott²,

Manjarín³

et al. 2014

Journal of Molecular Endocrinology

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Prolactin (PRL), acting via the PRL receptor (PRLR), controls hundreds of biological processes across a range of species. Endocrine PRL elicits well-documented effects on target tissues such as the mammary glands and reproductive organs in addition to coordinating wholebody homeostasis during states such as lactation or adaptive responses to the environment. While changes in PRLR expression likely facilitates these tissue-specific responses to circulating PRL, the mechanisms regulating this regulation in non-rodent species has received limited attention. We performed a wide-scale analysis of PRLR 5 0 transcriptional regulation in pig tissues. Apart from the abundantly expressed and widely conserved exon 1, we identified alternative splicing of transcripts from an additional nine first exons of the porcine PRLR (pPRLR) gene. Notably, exon 1.5 transcripts were expressed most abundantly in the heart, while expression of exon 1.3-containing transcripts was greatest in the kidneys and small intestine. Expression of exon 1.3 mRNAs within the kidneys was most abundant in the renal cortex, and increased during gestation. A comparative analysis revealed a human homologue to exon 1.3, hE1 N2 , which was also principally transcribed in the kidneys and small intestines, and an exon hE1 N3 was only expressed in the kidneys of humans. Promoter alignment revealed conserved motifs within the proximal promoter upstream of exon 1.3, including putative binding sites for hepatocyte nuclear factor-1 and Sp1. Together, these results highlight the diverse, conserved and tissue-specific regulation of PRLR expression in the targets for PRL, which may function to coordinate complex physiological states such as lactation and osmoregulation.

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Proliferation and mRNA expression of absorptive villous cell markers and mineral transporters in prolactin‐exposed IEC‐6 intestinal crypt cells

Cited by 9 publications

References 36 publications

Claudins in intestines

Claudins in intestines

Prolactin signaling enhances colon cancer stemness by modulating Notch signaling in a Jak2-STAT3/ERK manner

Comparative genomics reveals tissue-specific regulation of prolactin receptor gene expression

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