Estrogen-dependent regulation of sodium/hydrogen exchanger-3 (NHE3) expression via estrogen receptor β in proximal colon of pregnant mice

Choijookhuu, Narantsog; Sato, Yoko; Nishino, Tomoya; Endo, Daisuke; Hishikawa, Yoshitaka; Koji, Takehiko

doi:10.1007/s00418-012-0935-2

Cited by 23 publications

(17 citation statements)

References 57 publications

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“…Electric pulses (poring pulse: 75 V, 5 ms of length with 50-ms interval, transfer pulse: 20 V, 50 ms of length with 50-ms interval) were delivered using NEPA21 (Nepa Gene, Ichikawa, Japan). 57, 58 Knock-down effects were evaluated by western blotting.…”

Section: Methodsmentioning

confidence: 99%

CCL-1 in the spinal cord contributes to neuropathic pain induced by nerve injury

et al. 2013

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Cytokines such as interleukins are known to be involved in the development of neuropathic pain through activation of neuroglia. However, the role of chemokine (C-C motif) ligand 1 (CCL-1), a well-characterized chemokine secreted by activated T cells, in the nociceptive transmission remains unclear. We found that CCL-1 was upregulated in the spinal dorsal horn after partial sciatic nerve ligation. Therefore, we examined actions of recombinant CCL-1 on behavioural pain score, synaptic transmission, glial cell function and cytokine production in the spinal dorsal horn. Here we show that CCL-1 is one of the key mediators involved in the development of neuropathic pain. Expression of CCL-1 mRNA was mainly detected in the ipsilateral dorsal root ganglion, and the expression of specific CCL-1 receptor CCR-8 was upregulated in the superficial dorsal horn. Increased expression of CCR-8 was observed not only in neurons but also in microglia and astrocytes in the ipsilateral side. Recombinant CCL-1 injected intrathecally (i.t.) to naive mice induced allodynia, which was prevented by the supplemental addition of N-methyl-𝒟-aspartate (NMDA) receptor antagonist, MK-801. Patch-clamp recordings from spinal cord slices revealed that application of CCL-1 transiently enhanced excitatory synaptic transmission in the substantia gelatinosa (lamina II). In the long term, i.t. injection of CCL-1 induced phosphorylation of NMDA receptor subunit, NR1 and NR2B, in the spinal cord. Injection of CCL-1 also upregulated mRNA level of glial cell markers and proinflammatory cytokines (IL-1β, TNF-α and IL-6). The tactile allodynia induced by nerve ligation was attenuated by prophylactic and chronic administration of neutralizing antibody against CCL-1 and by knocking down of CCR-8. Our results indicate that CCL-1 is one of the key molecules in pathogenesis, and CCL-1/CCR-8 signaling system can be a potential target for drug development in the treatment for neuropathic pain.

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Section: Methodsmentioning

confidence: 99%

CCL-1 in the spinal cord contributes to neuropathic pain induced by nerve injury

et al. 2013

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“…In situ hybridization ISH was performed as described previously (Choijookhuu et al, 2012) using P5 wild-type mice. 45-base DNA antisense (coding nucleotides 432-476 in mouse Cdc42; 59-GCAGAGCACTCCACATACTTGAC-AGCCTTCAGATCCCGCGCCAGC-39) and sense (59-GCTGGCGCG-GGGATCTGAAGGCTGTCAAGTATGTGGAGTGCTCTGC-39) probes were labeled at their 59-end with digoxigenin-11-dUTP.…”

Section: Plasmidsmentioning

confidence: 99%

Maintenance of stereocilia and apical junctional complexes by Cdc42 in cochlear hair cells

Ueyama

Sakaguchi

Nakamura

et al. 2014

Journal of Cell Science

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BSTRACTCdc42 is a key regulator of dynamic actin organization. However, little is known about how Cdc42-dependent actin regulation influences steady-state actin structures in differentiated epithelia. We employed inner ear hair-cell-specific conditional knockout to analyze the role of Cdc42 in hair cells possessing highly elaborate stable actin protrusions (stereocilia). Hair cells of Atoh1-Cre;Cdc42 flox/flox mice developed normally but progressively degenerated after maturation, resulting in progressive hearing loss particularly at high frequencies. Cochlear hair cell degeneration was more robust in inner hair cells than in outer hair cells, and began as stereocilia fusion and depletion, accompanied by a thinning and waving circumferential actin belt at apical junctional complexes (AJCs). Adenovirus-encoded GFP-Cdc42 expression in hair cells and fluorescence resonance energy transfer (FRET) imaging of hair cells from transgenic mice expressing a Cdc42-FRET biosensor indicated Cdc42 presence and activation at stereociliary membranes and AJCs in cochlear hair cells. Cdc42-knockdown in MDCK cells produced phenotypes similar to those of Cdc42-deleted hair cells, including abnormal microvilli and disrupted AJCs, and downregulated actin turnover represented by enhanced levels of phosphorylated cofilin. Thus, Cdc42 influenced the maintenance of stable actin structures through elaborate tuning of actin turnover, and maintained function and viability of cochlear hair cells.

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“…The level of circulating estrogen may have an important role in the stimulation of estrogen signaling via ER␤ in the duodenal epithelium. In our previous study, the upregulation of sodium hydrogen exchanger-3 (NHE3) expression via ER␤ was found in mouse proximal colon, in parallel with the increase of circulating estrogen levels during pregnancy [34]. Moreover, circulating estrogen-dependent activation has been reported for both reproductive and non-reproductive organs [1,35].…”

Section: Discussionmentioning

confidence: 95%

“…Electroporatic transfection was performed as described previously [34]. Briefly, control or ER␤ siRNA were injected into the center of testis and three pulses (poring pulse: 40 V, 30 ms of length with 50 ms interval, transfer pulse: 25 V, 80 ms of length with 50 ms interval) were delivered into testis using Nepa21 electroporator (Nepa Gene, Chiba, Japan).…”

Section: Transfection Of Er␤ Sirna By Electroporationmentioning

confidence: 99%

Ontogenetic changes in the expression of estrogen receptor β in mouse duodenal epithelium

Choijookhuu

Hino

et al. 2015

Clinics and Research in Hepatology and Gastroenterology

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Estrogen-dependent regulation of sodium/hydrogen exchanger-3 (NHE3) expression via estrogen receptor β in proximal colon of pregnant mice

Cited by 23 publications

References 57 publications

CCL-1 in the spinal cord contributes to neuropathic pain induced by nerve injury

CCL-1 in the spinal cord contributes to neuropathic pain induced by nerve injury

Maintenance of stereocilia and apical junctional complexes by Cdc42 in cochlear hair cells

Ontogenetic changes in the expression of estrogen receptor β in mouse duodenal epithelium

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