Protein kinase C as a signal for exocytosis

Billiard, Julia; Koh, Duk Su; Babcock, Donner F.; Hille, Bertil

doi:10.1073/pnas.94.22.12192

Cited by 50 publications

(34 citation statements)

References 52 publications

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“…42 In other tissues, such as pituitary gonadotropes, exocytosis of secretory vesicles can be stimulated by activation of PKC independently of calcium elevation. 38 The mucin release induced by RELM␤ was inhibited by the PKC-specific inhibitory compound GF109203X, indicating that PKC is an important messenger. 43 As there is emerging evidence to suggest that tyrosine kinases may be involved in intestinal secretory processes, we investigated if they were important in RELM␤ mucosecretory action.…”

Section: Discussionmentioning

confidence: 98%

“…Since exocytosis of secretory vesicles can be stimulated independently either by calcium elevation or by activation of protein kinase C (PKC), 37,38 we first investigated whether RELM␤ had an effect on cytosolic calcium concentration of HT29-Cl.16E cells. RELM␤ did not mobilize cytosolic calcium, in contrast with the sharp response to Cch, shown in Figure 3A.…”

Section: Mechanism Of Relm␤ Mucosecretory Actionmentioning

confidence: 99%

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Resistin-like molecule β regulates intestinal mucous secretion and curtails TNBS-induced colitis in mice

Krimi

Kotelevets

Dubuquoy

et al. 2008

Inflammatory Bowel Diseases

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Section: Discussionmentioning

confidence: 98%

Section: Mechanism Of Relm␤ Mucosecretory Actionmentioning

confidence: 99%

Resistin-like molecule β regulates intestinal mucous secretion and curtails TNBS-induced colitis in mice

Krimi

Kotelevets

Dubuquoy

et al. 2008

Inflammatory Bowel Diseases

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“…Exocytosis can be stimulated either by increased concentrations of intracellular calcium or by increased PKC that is activated after incubation in phorbol 12-myristate 13-acetate (Billiard et al, 1997). Because PKC-␦ is a calcium-independent isoform (Azzi et al, 1992;Huang and Huang, 1993;Sossin and Schwartz, 1993), it would provide a regulatory signal for synaptic release that is independent of the calcium influx associated with excitation-secretion at synaptic terminals.…”

Section: Possible Role Of Pkc In Cerebellar Functionmentioning

confidence: 99%

Regional and cellular distribution of protein kinase C in rat cerebellar purkinje cells

2000

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Protein kinase C (PCK) is a family of isoforms that are implicated in subcellular signal transduction. The authors investigated the distribution of several PKC isoforms (PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon) within major cerebellar cell types as well as cerebellar projection target neurons, including Purkinje neurons, cerebellar nuclear neurons, and secondary vestibular neurons. PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon are found within the cerebellum. Of these isoforms, PKC-gamma and PKC-delta are highly expressed in Purkinje cells. PKC-gamma is expressed in all Purkinje cells, whereas the expression of PKC-delta is restricted to sagittal bands of Purkinje cells in the posterior cerebellar cortex. In the lower folia of the uvula and nodulus, Purkinje cell expression of PKC-delta is uniformly high, and the sagittal banding for PKC-delta expression is absent. Within the cerebellar nuclei, PKC-delta-immunolabeled axons terminate within the medial aspect of the caudal half of the ipsilateral interpositus nucleus. PKC delta-immunolabeled axons also terminated within the caudal medial and descending vestibular nuclei (MVN and DVN, respectively), the parasolitary nucleus (Psol), and the nucleus prepositus hypoglossi (NPH). PKC-gamma-immunolabeled axons terminated in all of the cerebellar nuclei as well as in the lateral and superior vestibular nuclei and the MVN, DVN, Psol, and NPH. The projection patterns of PKC-immunolabeled Purkinje cells were confirmed by lesion-depletion studies in which unilateral uvula-nodular lesions caused depletion of PKC-immunolabeled terminals ipsilateral to the lesion in the vestibular complex. These data identify circuitry that is unique to cerebellar-vestibular interactions.

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“…However, while the recruitment of particular coactivators may justify the differential effects of estrogenic compounds on gene expression activation in different cell types, it does not explain the different effects of a particular compound within the same cell. Intracellular messenger systems involved in LH secretion are sufficiently known: acute and chronic LH secretory responses to GnRH involve intracellular Ca 2+ increase and activation of protein kinase C [47, 48]. GnRH self-priming, which is a protein synthesis-dependent phenomenon [1, 49, 50], requires cAMP-protein kinase A system interaction with PR [50, 51, 52, 53]in the form of a ligand-independent activation of steroid receptor [54].…”

Section: Discussionmentioning

confidence: 99%

Tamoxifen but Not Other Selective Estrogen Receptor Modulators Antagonizes Estrogen Actions on Luteinizing Hormone Secretion while Inducing Gonadotropin-Releasing Hormone Self-Priming in the Rat

Sánchez-Criado

Guelmes²,

Bellido

et al. 2002

Neuroendocrinology

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Selective estrogen receptor modulators (SERMs) are compounds which may function as agonists or antagonists depending upon the target tissue. This study compares the actions of different SERMs on luteinizing hormone (LH) secretion, and on gonadotropin-releasing hormone (GnRH) self-priming in the rat. To do this, 4-day cyclic rats were injected twice, on day 2 (metestrus) and day 3 of the estrous cycle, with one of the following SERMs: 0.25 mg ICI 182,780, 3 mg tamoxifen (TX), LY139481-HCl or LY117018-HCl, or 0.5 mg RU58668. Control rats were given subcutaneous injections of 0.2 ml oil. On the morning of day 4 (proestrus in controls), rats from each group were either injected intraperitoneally with pentobarbital (40 mg/kg) for in vivo study or decapitated and their pituitaries collected for incubation (in vitro study). Additionally, pituitaries taken on each day of the estrous cycle from control rats as well as on day 4 from SERM-treated rats were processed for immunohistochemical determination of the estrogen receptor-α (ERα) gonadotrope. The plasma concentration or accumulation of LH in the medium was determined after 1 h (basal secretion). Thereafter, an intravenous bolus of GnRH (50 ng/0.5 ml/100 g BW) or 10^–8M GnRH was injected or added to the medium, respectively. After 1 h of GnRH exposure, blood or medium were taken, and another challenge of GnRH was made. At the end of the 3rd h of the experiment, blood or medium samples were taken again and the LH plasma concentration or accumulation in the medium were determined. All SERM treatments reduced uterus weight and decreased basal and stimulated LH secretion. Also, on day 4, rats treated with any SERM other than TX showed vaginal smears infiltrated by leukocytes and a reduction in GnRH self-priming. TX-treated rats exhibited cornified vaginal smears and an estrogenic effect on GnRH self-priming. Moreover, 15-min exposure to two consecutive GnRH (10^–8M) challenges 1 h apart in incubated pituitaries with estradiol (E₂, 10^–8M), TX (10^–7M), E₂ + TX, or medium alone form ovariectomized rats injected for 3 days with estradiol benzoate (25 µg), TX (3 mg), estradiol benzoate + TX, or 0.2 ml oil, respectively, showed that TX increased GnRH self-priming, as did E₂, whereas it reduced the E₂-sensitizing effect on GnRH-stimulated LH secretion and cancelled the E₂-dependent GnRH self-priming. All SERMs prevented the physiological nucleocytoplasmic shuttling of ERα exhibited during proestrus in control rats, and TX, in addition, induced a significantly larger number of gonadotropes displaying strong cytosolic immunosignals corresponding to ERα than the rest of the experimental groups. Overall, data from this study indicated that, in contrast to the general antagonistic effect of the tested SERMs, TX seemed to display both selective agonist and antagonist activity at the gonadotrope level and on GnRH self-priming of LH secretion respectively.

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Protein kinase C as a signal for exocytosis

Cited by 50 publications

References 52 publications

Resistin-like molecule β regulates intestinal mucous secretion and curtails TNBS-induced colitis in mice

Resistin-like molecule β regulates intestinal mucous secretion and curtails TNBS-induced colitis in mice

Regional and cellular distribution of protein kinase C in rat cerebellar purkinje cells

Tamoxifen but Not Other Selective Estrogen Receptor Modulators Antagonizes Estrogen Actions on Luteinizing Hormone Secretion while Inducing Gonadotropin-Releasing Hormone Self-Priming in the Rat

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