Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated effects of various agents on proliferation, intracellular pH (pHi), and intracellular calcium [( Ca2+]i) of rat mesangial cells (MCs) in early passages (2-5). Serum-starved MCs incubated in HCO3- were exposed to one of the following: fetal calf serum (FCS), serotonin, angiotensin II (ANG II), arginine vasopressin (AVP), bombesin (Bom), bradykinin (BK), epidermal growth factor (EGF), epinephrine (Epi), interleukin 1 (IL-1), norepinephrine (NE), neuropeptide Y, oxytocin, substance P (SP), platelet-derived growth factor, or 12-O-tetradecanoylphorbol-13-acetate (TPA). We assessed DNA synthesis from [3H]thymidine uptake during exposure to test agent. All agents except ANG II, NE, Bom, and SP were mitogenic. When MCs were incubated in a HCO3(-) -free N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered medium, maximal mitogenic responses to FCS, AVP, and EGF were 41, 44, and 55% (P less than 0.01) lower, respectively, than those in presence of HCO3-. In absence of HCO3-, agents other than BK and IL-1 produced a biphasic pHi response characterized by a transient acidification followed by a prolonged alkalinization that was both Na(+)-dependent and amiloride-sensitive. In presence of HCO3-, agents produced only a small and gradual acidification, except for IL-1 and Epi. Addition of all agonists except IL-1, EGF, and TPA produced significant transient increases in [Ca2+]i, the magnitudes of which were similar in HCO3- and non-HCO3- buffers. These results demonstrate that, in presence of HCO3-, agents (i.e., NE and ANG II) can produce typical [Ca2+]i transients and still not cause MC proliferation. Conversely, an agent may cause proliferation without eliciting a short-term change in either [Ca2+]i or pHi (i.e., IL-1), a change in [Ca2+]i but not pHi (i.e., Epi), or a change in pHi but not [Ca2+]i (i.e., TPA). Thus, at least for MCs, proliferation in HCO3- can be dissociated from early agonist-induced changes in pHi and [Ca2+]i.
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PMID:Effects of mitogens and other agents on rat mesangial cell proliferation, pH, and Ca2+. 211 98

This experiment was designed to study the effects of cell-to-cell contact, arachidonic acid (10 microM; AA), oxytocin (10 microM), and luteinizing hormone (5 ng; LH) on bovine luteal cell function. Corpora lutea collected from Holstein cows between Days 10 and 12 (n = 4; midluteal stage) or 17 and 18 (n = 4; late-luteal stage) of the estrous cycle (Day 0 = estrus) were dispersed, and small and large cells were separated by unit gravity sedimentation and flow cytometry. Large and small luteal cells were either incubated together, allowing intercellular contact, or separately, without intercellular contact, with culture well inserts. Cells were incubated in a modified Ham's F-12-N-hydroxyethylpiperazine-N'-2-ethanesulfonic acid medium. After an 18-hr preincubation period, treatments were introduced and cells were incubated for 240 hr. Media samples were collected and treatments were replaced at 48-hr intervals. Incubations were maintained at 37 degrees C in 5% CO2 in humidified air. Overall, progesterone secretion decreased with increased incubation time (P < 0.0001), regardless of treatment, stage of the cycle, or cell arrangement. During the 18-hr pretreatment period, large and small luteal cells with contact secreted more progesterone than did luteal cells without contact during both the mid- (P < 0.0001) and late-luteal stages (P < 0.06) of the estrous cycle. After treatments were initiated, both mid- and late-stage luteal cells treated with LH secreted more (P < 0.0001) progesterone than occurred with any other treatment; oxytocin, AA, and control treatments were similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contact-associated interactions between large and small bovine luteal cells during the estrous cycle. 762 77