Prolactin is involved in glial responses following a focal injury to the juvenile rat brain

Möderscheim, Tanja A.E.; Gorba, Thorsten; Pathipati, Praneeti; Kokay, Ilona C.; Grattan, David R.; Williams, Chris; Scheepens, Arjan

doi:10.1016/j.neuroscience.2006.12.053

Cited by 57 publications

(31 citation statements)

References 51 publications

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“…Moreover, the present results confirm previous findings (Huerta-Ocampo, 2007;Mena et al, 2010;Mena et al, 2011;Möderscheim et al, 2007, Mena et al, 2012a, that CM from lactating rats, contain prolactin variants capable of inducing rapid release of PRL from the untreated male rat pituitary, and that they can also activate of astrocytes and neurons in different areas of the central and peripheral nervous system (Mena et al, 2012b …”

Section: Discussionsupporting

confidence: 92%

“…Several reports indicate that PRL has some neuro and gliatrophic properties, and that it mediates the development and maturation of dopaminergic neurons in the hypothalamopituitary system (Möderscheim et al, 2007). We showed previously (Morales et al, 2001) that intrathecal injection of PRL in the spinal cord promoted the sympathetic inhibition of milk ejection in lactating rats, and that prolactin variants in CM from the central and peripheral regions of the anterior pituitary from lactating, but not from male rats promoted the in vitro release of PRL from pituitary glands of male rats in a dose-dependent manner (Huerta-Ocampo et al, 2007;Mena et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Autocrine and Paracrine Regulation of Prolactin Secretion by Prolactin Variants and by Hypothalamic Hormones

Mena¹,

Navarro²,

Castilla³

2013

Prolactin

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Autocrine and Paracrine Regulation of Prolactin Secretion by Prolactin Variants and by Hypothalamic Hormones

Mena¹,

Navarro²,

Castilla³

2013

Prolactin

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“…These findings imply that the physiological levels of PRL are mildly antinociceptive, and inflammation-induced PRL levels have hyperalgesic effects. Interestingly, systemic and prolonged treatments with supraphysiological concentrations of PRL, which are observed during lactation in females, could provide a protective effect for certain cell types (1,50). This dual-effect phenomenon is reported for many trophic factors, and PRL could play such a role.…”

Section: Discussionmentioning

confidence: 96%

“…TRPV1 and TRPA1 play a role in inflammatory mechanical allodynia possibly via presynaptic mechanisms in the dorsal spinal cord (32,57). A direct action of PRL on TRPs at the same site is possible, since activated microglia could release PRL during inflammation where this release could also contribute to the development of inflammatory hyperalgesia (50). Second, elevated levels of endogenous PRL during inflammation in the spinal cord could transiently sensitize channels at postsynaptic sites, resulting in enhanced neuronal activities.…”

Section: Discussionmentioning

confidence: 99%

Prolactin regulates TRPV1, TRPA1, and TRPM8 in sensory neurons in a sex-dependent manner: Contribution of prolactin receptor to inflammatory pain

Patil

Ruparel

Henry

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

113

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Patil MJ, Ruparel SB, Henry MA, Akopian AN. Prolactin regulates TRPV1, TRPA1, and TRPM8 in sensory neurons in a sex-dependent manner: Contribution of prolactin receptor to inflammatory pain. Am J Physiol Endocrinol Metab 305: E1154-E1164, 2013. First published September 10, 2013; doi:10.1152/ajpendo.00187.2013 is a hormone produced in the anterior pituitary but also synthesized extrapituitary where it can influence diverse cellular processes, including inflammatory responses. Females experience greater pain in certain inflammatory conditions, but the contribution of the PRL system to sexdependent inflammatory pain is unknown. We found that PRL regulates transient receptor potential (TRP) channels in a sex-dependent manner in sensory neurons. At Ͼ20 ng/ml, PRL sensitizes TRPV1 in female, but not male, neurons. This effect is mediated by PRL receptor (PRL-R). Likewise, TRPA1 and TRPM8 were sensitized by 100 ng/ml PRL only in female neurons. We showed that complete Freund adjuvant (CFA) upregulated PRL levels in the inflamed paw of both male and female rats, but levels were higher in females. In contrast, CFA did not change mRNA levels of long and short PRL-R in the dorsal root ganglion or spinal cord. Analysis of PRL and PRL-R knockout (KO) mice demonstrated that basal responses to cold stimuli were only altered in females, and with no significant effects on heat and mechanical responses in both sexes. CFA-induced heat and cold hyperalgesia were not changed in PRL and PRL-R KO compared with wild-type (WT) males, whereas significant reduction of heat and cold post-CFA hyperalgesia was detected in PRL and PRL-R KO females. Attenuation of CFA-induced mechanical allodynia was observed in both PRL and PRL-R KO females and males. Thermal hyperalgesia in PRL KO females was restored by administration of PRL into hindpaws. Overall, we demonstrate a sex-dependent regulation of peripheral inflammatory hyperalgesia by the PRL system. prolactin receptor; transient receptor potential V1; transient receptor potential A1; transient receptor potential M8; female; inflammation; pain MANY HUMAN CHRONIC INFLAMMATORY conditions are associated with hyperprolactinemia, and this increase in prolactin (PRL) levels can lead to serious health issues related to cancer, infertility, inflammatory diseases, and body weight (11,42,48,73). Human inflammatory conditions with increased PRL serum levels include the severe form of progressive systemic sclerosis (34, 69), the active phase of systemic lupus erythematosus (37, 74), rheumatoid arthritis (44), polymyalgia rheumatica (68), and autoimmune thyroid diseases (26). Unlike chronic inflammation, acute inflammation in animals triggers an accumulation of endogenous PRL at the site of inflammation, but not in blood serum (64). Altogether, these findings suggest that acute inflammation upregulates PRL via extrapituitary mechanisms, whereas chronic inflammation induces PRL via both pituitary and extrapituitary pathways (64, 75).Elevated PRL can have modulatory effects on metabolic/ endocrine and the ...

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“…sodium pump; energy depletion; sodium azide; 2,4-dinitro phenol; Jurkat T cells; Janus kinase 2 THE JANUS KINASE-2 (JAK2)-signal transducer and activator of transcription-5 (STAT5) pathway participates in the signaling of several hormones including leptin (61), erythropoietin (23,45,71,85), and growth hormone (15,16). Leptin (7,76), erythropoietin (60) and growth hormone (24,57) are in turn known to protect cells against ischemic cell injury. Cell survival during energy depletion critically depends on electrolyte transport across the cell membrane (47), as ATP is required for the function of the Na ϩ /K ϩ -ATPase (75).…”

mentioning

confidence: 99%

Energy-sensitive regulation of Na⁺/K⁺-ATPase by Janus kinase 2

Bhavsar

Hosseinzadeh

Brenner

et al. 2014

American Journal of Physiology-Cell Physiology

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Janus kinase 2 (JAK2) contributes to intracellular signaling of leptin and erythropoietin, hormones protecting cells during energy depletion. The present study explores whether JAK2 is activated by energy depletion and regulates Na+/K+-ATPase, the major energy-consuming pump. In Jurkat cells, JAK2 activity was determined by radioactive kinase assay, phosphorylated JAK2 detected by Western blotting, ATP levels measured by luciferase assay, as well as Na+/K+-ATPase α1-subunit transcript and protein abundance determined by real-time PCR and Western blotting, respectively. Ouabain-sensitive K+-induced currents ( Ipump) were measured by whole cell patch clamp. Ipump was further determined by dual-electrode voltage clamp in Xenopus oocytes injected with cRNA-encoding JAK2, active V617FJAK2, or inactive K882EJAK2. As a result, in Jurkat T cells, JAK2 activity significantly increased following energy depletion by sodium azide (NaN3) or 2,4- dinitro phenol (DNP). DNP- and NaN3-induced decrease of cellular ATP was significantly augmented by JAK2 inhibitor AG490 and blunted by Na+/K+-ATPase inhibitor ouabain. DNP decreased and AG490 enhanced Ipump as well as Na+/K+-ATPase α1-subunit transcript and protein abundance. The α1-subunit transcript levels were also enhanced by signal transducer and activator of transcription-5 inhibitor CAS 285986-31-4. In Xenopus oocytes, Ipump was significantly decreased by expression of JAK2 and V617FJAK2 but not of K882EJAK2, effects again reversed by AG490. In V617FJAK2-expressing Xenopus oocytes, neither DNP nor NaN3 resulted in further decline of Ipump. In Xenopus oocytes, the effect of V617FJAK2 on Ipump was not prevented by inhibition of transcription with actinomycin. In conclusion, JAK2 is a novel energy-sensing kinase that curtails energy consumption by downregulating Na+/K+-ATPase expression and activity.

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Prolactin is involved in glial responses following a focal injury to the juvenile rat brain

Cited by 57 publications

References 51 publications

Autocrine and Paracrine Regulation of Prolactin Secretion by Prolactin Variants and by Hypothalamic Hormones

Autocrine and Paracrine Regulation of Prolactin Secretion by Prolactin Variants and by Hypothalamic Hormones

Prolactin regulates TRPV1, TRPA1, and TRPM8 in sensory neurons in a sex-dependent manner: Contribution of prolactin receptor to inflammatory pain

Energy-sensitive regulation of Na⁺/K⁺-ATPase by Janus kinase 2

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Prolactin is involved in glial responses following a focal injury to the juvenile rat brain

Cited by 57 publications

References 51 publications

Autocrine and Paracrine Regulation of Prolactin Secretion by Prolactin Variants and by Hypothalamic Hormones

Autocrine and Paracrine Regulation of Prolactin Secretion by Prolactin Variants and by Hypothalamic Hormones

Prolactin regulates TRPV1, TRPA1, and TRPM8 in sensory neurons in a sex-dependent manner: Contribution of prolactin receptor to inflammatory pain

Energy-sensitive regulation of Na+/K+-ATPase by Janus kinase 2

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Product

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About

Energy-sensitive regulation of Na⁺/K⁺-ATPase by Janus kinase 2