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PubMed1991

Metabolic effects of growth factors and polycyclic aromatic hydrocarbons on cultured human placental cells of early and late gestation.

The metabolic effects of epidermal growth factor (EGF), insulin, insulin-like growth factor-I (IGF-I), and IGF-II were determined on human placental cells in monolayer culture obtained from early gestation (less than 20 weeks) and late gestation (38-42 weeks). Parameters studied were uptake of aminoisobutyric acid (AIB), uptake of 3-O-methylglucose and [3H]thymidine incorporation into cell protein. Since benzo[alpha]pyrene (BP) inhibits EGF binding and autophosphorylation in cultured human placental cells, particularly in early gestation, we also studied the effect of benzo[alpha]pyrene and other polycyclic aromatic hydrocarbons (PAHs) on EGF-mediated AIB uptake. The metabolic effects of EGF, insulin, and the IGFs in cultured human placental cells varied with gestational age and the growth factor studied. All three classes of growth factors stimulated AIB uptake in both early and late gestation at concentrations from 10-100 micrograms/L, well within a physiological range. However, insulin stimulation of AIB uptake was maximal at a high concentration (200 micrograms/L) in both early and late gestation cells, suggesting an action via type 1 IGF receptors rather than via insulin receptors. EGF stimulated 3-O-methylglucose uptake only in term placental cells. No significant stimulation of [3H]thymidine incorporation by any of the growth factors tested was seen with either early or late gestation cells. The effect of PAHs on AIB uptake by cultured placental cells was variable. BP alone stimulated AIB uptake by both very early and late gestation cells and enhanced EGF-stimulated AIB uptake. alpha-naphthoflavone alone inhibited AIB uptake at all gestational ages and inhibited EGF-stimulated AIB uptake. beta-Naphthoflavone and 3-methylcholanthrene minimally inhibited AIB uptake by early gestation cells and did not modify EGF-stimulated uptake at any gestational period. Our prior results demonstrated that BP more significantly inhibited EGF than IGF or insulin receptor binding as well as autophosphorylation in early gestation placenta, and that BP was the most potent of the PAHs tested. Thus, the direct effect of the PAHs on placental EGF receptors and amino acid transport may indicate altered function of EGF in the regulation of placental growth in smoking mothers that is developmentally regulated.

Aminoisobutyric Acids↗
PubMed1984

The type I insulin-like growth factor receptor mediates the rapid effects of multiplication-stimulating activity on membrane transport systems in rat soleus muscle.

Multiplication-stimulating activity (MSA) stimulates the uptake of xylose and alpha-aminoisobutyric acid (AIB) by intact rat soleus muscle. It is approximately 50 times less potent than insulin. A native insulin receptor species with apparent Mr = 350,000 in soleus muscle is revealed by affinity cross-linking to 125I-insulin with disuccinimidyl suberate. 125I-labeled insulin-like growth factor (IGF) I with the cross-linker affinity labels two native receptor types with Mr = 360,000 (type I) and Mr = 220,000 (type II). In order to distinguish which of the three insulin and IGF receptor systems identified mediate the rapid insulin-like effects of MSA, the biological actions of the unlabeled ligands at various concentrations were correlated with their ability to inhibit the affinity labeling of these receptor species. The stimulatory action of native insulin is closely related to its ability to inhibit the labeling of the insulin receptor by 125I-insulin such that the uptake of xylose and AIB is maximally stimulated when 80% of insulin receptor 125I-affinity labeling is inhibited. In contrast, MSA only displaced 16% of the 125I-labeling of the insulin receptor when it maximally stimulates the uptake of xylose and AIB, indicating that the insulin receptor is not primarily involved in mediating these effects. The affinity of MSA to the type II IGF receptor is 10 times higher than that to the type I IGF receptor. There is close to a 1:1 relationship between the stimulatory effects of MSA on xylose and AIB uptake and its inhibitory action on the affinity labeling of the type I receptor by 125I-IGF I. In contrast, MSA almost abolishes the labeling of the type II IGF receptor at concentrations which have no detectable effects on the uptake of xylose and AIB by soleus muscle. Thus, a marked dissociation can be observed between the rapid insulin-like action of MSA and its inhibitory effects on the affinity labeling of the type II receptor by 125I-IGF I. We conclude that MSA acts through the type I IGF receptor in soleus muscle to stimulate hexose and amino acid transport. The type II IGF receptor appears to be incapable of modulating these effects in this tissue.

Aminoisobutyric Acids↗
PubMed1990

Inhibition of sodium-dependent L-leucine uptake in rat brain synaptosomes.

Synaptosomes isolated from adult rat cerebral cortices were used for studying the uptake of L-leucine by the Na(+)-dependent route. Three non-metabolizable amino acid analogues, which had been used previously to discriminate the Na(+)-dependent A-type uptake system of animal cells, were employed in this study. It was found that Na(+)-dependent uptake of leucine was insensitive to inhibition by 2-aminoisobutyric acid (AIB) and N-methylaminoisobutyric acid (MeAIB) whereas N-methylalanine (NMA) was markedly inhibitory. Inhibition by NMA was stereospecific--only the L-isomer had a pronounced effect. Na(+)-dependent uptake of leucine as well as its inhibition by L-NMA were rather insensitive to changes in pH from 6 to 9. Kinetic analysis of inhibition by L-NMA of Na(+)-dependent uptake revealed a non-competitive type of inhibition with a Ki value of approximately 0.5 mM.

Alanine↗
PubMed1978

The effect of chondrocyte growth factor on membrane transport by articular chondrocytes in monolayer culture.

Chondrocyte growth factor (CGF), a contaminant of pituitary glycoprotein hormones, stimulates growth of cultured lapine articular chondrocytes while depressing SO4-proteoglycan synthesis. To study its effect on membrane transport, NIH-bTSH and two other preparations with comparable CGF activity were employed. In early log phase (36 hr) cultures CGF (64 microgram/ml) did not alter thymidine (dThd) uptake during the first 5 min. By 15 min however, TCA-precipitable dThd was 4-fold greater than in controls while the TCA-soluble fraction remained the same. CGF increased deoxy-glucose (DG) uptake in 36-hr old cultures. At 66 hr, CGF reduced DG transport. The transport of cycloleucine (CL) and aminoisobutyric acid (AIB) was reduced by CGF in 36 and 66-hr old cultures. There was a dose dependency between CGF concentration, the lowered uptake of DG, CL and AIB, and cell protein content. The effect of CGF on DG transport and dThd incorporation into DNA was not immediate but required prior exposure of the cells to CGF. CGF did not alter DG transport in rabbit or mouse fibrocytes or Chang liver cells. This and the reported finding that pituitary fibroblast growth factor (FGF), increases amino acid transport in other cells suggests that the biological specificity of CGF may not be identical to that of FGF.

Aminoisobutyric Acids↗
PubMed1983

Blood-brain barrier changes with kainic acid-induced limbic seizures.

Rats were treated with kainic acid (KA) i.v. to produce increasingly severe limbic seizures that were monitored with a behavioral rating scale. At various times after the induction of seizures, the animals; blood-brain barriers (B-BB) were studied with alpha-[14C]aminoisobutyric acid ([14C]AIBA) autoradiography. Using optical density ratios, a coefficient was devised to assess the functional integrity of the B-BB in discrete anatomic regions and to quantitatively compare these measurements among different groups of experimental animals. In animals that exhibited only mild seizures, the B-BB was not different from controls. Animals with severe limbic seizures, however, showed alterations. For as long as 2 h after delivery of KA, the B-BB appeared normal; from 2 to 24 h, the permeability to [14C]AIBA was markedly increased throughout the brain, especially in limbic regions; from 24 h to 7 days the B-BB returned to normal except for a small residual change in limbic structures. These findings were confirmed with Evans blue dye studies of the B-BB. A correlation between focal accentuation of B-BB alterations and neuropathologic changes was found. These experiments indicted that recurrent limbic seizures may lead to a breakdown in the B-BB independent of systemic metabolic derangements. Marked focal metabolic and electrical changes, however, occurred in several limbic structures several hours before the blood-brain barrier was altered.

Aminoisobutyric Acids↗
PubMed1986

Renal tubular transport of delta-aminolevulinic acid in rat.

delta-Aminolevulinic acid (ALA) interferes with cell membrane and metabolic functions in a variety of tissues. To determine if ALA interacts with renal tubular transport functions, we examined concentrative transport of this heme precursor in rat kidneys. ALA was accumulated against a concentration gradient in rat renal cortical slices. Section freeze-dry autoradiography demonstrated selective accumulation in cells of proximal tubules. Concentrative uptake of ALA was inhibited by KCN, probenecid and p-aminohippurate (PAH). ALA inhibited slice uptake of PAH but failed to block slice accumulation of galactose, cycloleucine, lysine, glycine, proline, or alpha-aminoisobutyric acid and did not alter O2 utilization. Massive intraperitoneal injection of ALA did not increase 24 hr fractional excretion of amino acids in vivo. Concentrative transport of ALA in proximal tubules does not lead to generalized renal tubular transport defects but ALA appears to share the organic acid secretory system in rat kidney.

Aminoisobutyric Acids↗
PubMed1979

Amino acid and 22Na+ uptake in membrane vesicles from confluent simian virus 40 transformed Balb/c3T3 and Balb/c3T3.

The studies reported here were carried out to characterize further previously described changes in membrane localized amino acid transport associated with simian virus 40 transformation of the mammalian cell line, Balb/c3T3. Membrane vesicles were prepared from confluent cultures of both simian virus 40 transformed Balb/c3T3 (SV3T3) and the untransformed parent line, Balb/c3T3 (3T3). An initial, externally imposed out greater than in, 100 mM a+ gradient produces acceleration of early ingress of alpha-aminoisobutyric acid (AlB) in vesicles from both cell lines, but transient, concentrative uptake (overshooting) only in SV3T3 vesicles. Early ingress of L-leucine is also accelerated in SV3T3 vesicles by a Na+ gradient, and overshooting is also demonstrable. Na+-gradient independent AIB permeability of SV3T3 and 3T3 membranes was estimated using uptake data, a first order rate equation and measurements of vesicle size derived from quasi-elastic light-scattering studies. AIB permeability of SV3T3 membranes is greater than that of 3T3 membranes (113 A/min and 43 A/min, respectively), suggesting that overshooting in 3T3 vesicles is not attenuated by a Na+-independent AIB "leak". Na+ permeability of the two membranes is similar, ruling out the possibility that a slower rate of Na+ equilibration across the SV3T3 membrane allows development of the overshoot. In SV3T3 vesicles the height of a Na+-gradient dependent overshoot varies with the initial [Na+]o/[Na+]i ratio, and ln[Na+]o/[Na+]i is linearly related to ln AIB uptake at overshoot peak/AIB uptake at equilibrium, consistent with the possibility that for [Na+]o/[Na+]i ratios in the range studied, AIB overshoot is energized by a constant proportion of the energy available from the initial electrochemical gradient for Na+. These results are consistent with the possibility that Na+-gradient dependent overshooting in SV3T3 vesicles is produced by Na+-amino acid carrier interactions resulting in either an increase in maximum transport velocity or an increase in carrier affinity for AIB.

Aminoisobutyric Acids↗
PubMed1982

Insulin and glucagon binding and stimulation of amino acid transport in isolated hepatocytes from streptozotocin diabetic rats.

The binding of insulin and glucagon and the effects of these hormones on amino acid transport were examined in isolated rat hepatocytes from streptozotocin diabetic rats. Hepatocytes from diabetic rats bound more insulin than cells from control animals. These changes were accounted for by a 50%-60% increase in the number of insulin receptors per cell. Glucagon binding did not significantly differ in hepatocytes from both groups. Following a 2 hr incubation of the cells in vitro, the basal rate of alpha-aminoisobutyric acid (AIB) influx was enhanced in diabetic rat hepatocytes compared to controls. This alteration was accounted for by an increase in the Vmax of both a low affinity and a high affinity component of transport. The ability of diabetic rat hepatocytes to respond to maximally stimulating concentrations of insulin or glucagon by enhancing further the rate of AIB influx was markedly diminished. Hormone responsiveness was restored to normal in hepatocytes from insulin-treated diabetic animals. The data suggest that in diabetic rat hepatocytes the diminished insulin and glucagon responsiveness with regard to the stimulation of amino acid transport stems from postreceptor alteration(s).

Aminoisobutyric Acids↗
PubMed1987

Insulin-like growth factor II binding and action in human fetal fibroblasts.

To investigate the role of insulin-like growth factor II (IGF-II) in human prenatal growth, IGF-II binding and biological action were studied in four lines of fetal and three lines of postnatal human fibroblasts. Specific binding of IGF-II was similar in both groups: 15.7% and 14.9% for fetal and postnatal fibroblasts, respectively. This was 5-10 times the amount of IGF-I binding found in these cells. IGF-I and IGF-II caused dose-dependent increases in [14C]aminoisobutyric acid (AIB) uptake. IGF-II was sevenfold less potent than IGF-I in stimulating this metabolic response in both fetal and postnatal fibroblasts. The maximal effect of IGF-II in stimulating [14C]AIB uptake approach that of IGF-I. Similar results were obtained when IGF-I and IGF-II stimulation of [3H]thymidine incorporation was compared in fetal and postnatal fibroblasts. Incubation in the presence of alpha IR-3, a monoclonal antibody to the type I IGF receptor, inhibited the ability of both IGF-I and IGF-II to stimulate [14C]AIB uptake and [3H]thymidine incorporation in fetal and postnatal cells. A monoclonal antibody to the insulin receptor did not affect IGF action. These data indicate that IGF-II is a potent metabolic and mitogenic stimulus for human fetal fibroblasts. However, despite the presence of abundant type II IGF receptors on both fetal and postnatal human fibroblasts, IGF-II stimulation of amino acid transport and DNA synthesis appears to be mediated through the type I rather than through its own type II IGF receptor.

Aminoisobutyric Acids↗
PubMed1997

Giardia intestinalis: volume recovery in response to cell swelling.

The trophozoite from of the protozoan parasite Giardia intestinalis is subjected to a changing osmotic environment in the small intestine of the host, and consequently effective osmoregulation and control of cell volume are essential to its survival. As a first step toward investigating the mechanism by which hypoosmotically-activated transport is controlled in this organism, we used a light scattering technique to monitor continuously changes in cell volume after osmotic challenge. There was a hyperbolic relationship between A550 and giardial protein concentration, resulting in linear double reciprocal plots and allowing the calculation of relative Giardia cell volumes from A550 values. The initial rate of cell swelling was directly proportional to the hypoosmotic gradient when the hypoosmotic difference was greater than 50 mOsm kg-1. However, a hypoosmotic challenge of < 30 mOsm kg-1 had little effect on cell swelling, suggesting that giardial cell rigidity can resist small changes in medium osmolarity. The use of light scattering as a measure of giardial cell volume changes was validated using a rapidly penetrating solute, ethylene glycol, to induce isoosmotic cell swelling. We have previously shown that trophozoites swelled initially when subjected to a hypoosmotic challenge and that a subsequent regulatory volume decrease was accompanied by rapid alanine efflux and activation of the uptake of an alanine analog, 2-aminoisobutyrate. The ethylene glycol-induced isoosmotic cell swelling was also followed by a regulatory volume decrease, accompanied by a similar rapid release of intracellular alanine and activation of 2-aminoisobutyric acid uptake. This suggests that an increase in cell volume is the primary stimulus for the rapid alanine efflux after hypoosmotic challenge.

Alanine↗
PubMed1980

Intraneuronal effects of inhibitory amino acids.

Injections of gamma-aminobutyric acid (GABA) into spinal motoneurons (in cats under Dial) induce a small but relatively prolonged hyperpolarization (mean - 1.7 mV, SD 2.1; n = 25) which is associated with a rise in input resistance (mean 44%, SD 122; n = 34), is not reversed by hyperpolarization, and is not potentiated by intracellular release of benzodiazepines. Muscimol sometimes has a comparable effect, but alpha-aminoisobutyric acid and glycine do not. These observations are consistent with the possibility that motoneurons have a Na+-coupled GABA transport mechanism that is electrogenic and can be reversed by an excess of intracellular GABA.

Action Potentials↗
PubMed1983

Specificity and control of uptake of purines and other compounds in Bacillus subtilis.

Certain nucleotides control adaptation to changing nutrition or differentiation (sporulation) resulting from a general nutritional deficiency. To maintain the adaptation or differentiation process, once it has started, it may have been important for cells to evolve several independent and metabolically controllable systems enabling the uptake and metabolism of various nucleic acid bases or nucleosides. We have analyzed the cellular reactions with these compounds by measuring both their effect on growth and their uptake in appropriately chosen auxotrophic and uptake mutants. We have found one uptake system for guanine and hypoxanthine, another one for guanosine and inosine, and three other systems for adenine, adenosine, and uracil. The uptake systems of guanine-hypoxanthine and guanosine-inosine are inhibited by the stringent response to amino acid deprivation (increase of guanosine 5'-diphosphate-3'-diphosphate), but they do not depend on the concentration of GTP, which decreases during sporulation. In contrast, the uptake of Ura depends on the presence of GTP, regardless of whether a GTP decrease was produced by the stringent response or otherwise. This was the only uptake system whose decrease was always correlated with the onset of sporulation. The uptake of other compounds, e.g., alpha-methylglucoside and alpha-aminoisobutyric acid, decreased under some, but not all, sporulation conditions.

Adenine↗
PubMed1986

In vitro damage to rat lens by xanthine-xanthine oxidase: protection by ascorbate.

The potential of ascorbic acid acting against the toxic effects of active oxygen species on the lens has been studied. The active species of oxygen were generated by the action of xanthine oxidase on xanthine. Rat lenses incubated in medium containing xanthine and xanthine oxidase were physiologically damaged, as evidenced by the decrease in the ability of the tissue to accumulate rubidium or alpha-aminoisobutyric acid against a concentration gradient. The pressure of ascorbate in the medium protected against the tissue damage. One of the functions of high ascorbate in the aqueous humor of many primates including human beings may, therefore, be to protect the lens and other surrounding tissues against the toxic effects of active oxygen derivatives produced in situ under ambient, as well as under photochemical, conditions.

Aminoisobutyric Acids↗
PubMed1970

Energy coupling in the lactose transport system of Escherichia coli.

A mutant (ML 308-22) was isolated from Escherichia coli ML 308, which had lost the normal capacity to accumulate lactose analogs despite an increase in the membrane carrier activity. The exit of thiomethylgalactoside was much faster than normal, accounting for the inability of the cell to maintain high intracellular concentrations of galactosides. Growth of the mutant on lactose was normal at high concentrations of sugar and impaired at low concentrations. This transport defect appeared to be limited to the lactose transport system as D-fucose and alpha-aminoisobutyric acid uptake and accumulation were normal. It is inferred from the data that the mutant possessed a defect in the coupling of metabolic energy to lactose transport.

Aminoisobutyric Acids↗
PubMed1991

[Metabolic and mitogenic effects of insulin-like growth factor I on rat glomerular mesangial cells cultured under high concentration of glucose].

Recent studies indicate the important roles of mesangial cell dysfunction and insulin-like growth factor I (IGF-I) in the development of diabetic nephropathy. In order to know whether hyperglycemia could alter IGF-I action on mesangial cells, we examined mitogenic and metabolic effects of IGF-I on mesangial cells. Mesangial cells revealed to express considerable numbers of receptors specific to IGF-I will relatively small numbers of insulin receptors. The uptake of [3H]-2-deoxy-glucose, [3H]-aminoisobutyric acid (AIB), or [3H]-thymidine into mesangial cells was stimulated by IGF-I at physiological concentrations. Under high concentrations of glucose (55 mM), the stimulation of thymidine uptake by IGF-I was significantly suppressed from 5863 +/- 549 (at 11 mM glucose) to 1731 +/- 146 DPM/100 micrograms/prot. On the contrary, AIB incorporation by IGF-I was significantly enhanced in the cells cultured under high concentration of glucose, as 2.03 +/- 0.03n mol/mg protein/15 min at 55 mM glucose vs 0.59 +/- 0.01 at 11 mM glucose. In conclusion; 1) IGF-I had metabolic and mitogenic effects on rat mesangial cells at physiological concentrations. 2) under excess glucose conditions, mitogenic action of IGF-I on rat mesangial cells was suppressed, while amino acid incorporation was enhanced. These results suggest that modulation of IGF-I effects on mesangial cell by glucose could be associated with mesangial cell dysfunction in diabetes.

Aminoisobutyric Acids↗
PubMed1980

Insulin action and binding in isolated hepatocytes from fasted, streptozotocin-diabetic, and older, spontaneously obese rats.

Insulin binding and basal and insulin-stimulated uptake of alpha-aminoisobutyric acid were measured in isolated hepatocytes from young control rats as well as from older spontaneously obese, 72h-starved, and nonketotic streptozotocin-diabetic rats. Isolated hepatocytes from older spontaneously obese rats are similar to those from younger smaller rats in size, maximal insulin responsiveness, the dose-response relationship for insulin-stimulated aminoisobutyrate uptake, and the number and affinity of insulin receptors. Hepatocytes from 72h-fasted rats have similar numbers of insulin receptors per cell as cells from young control animals, but are significantly smaller, have an enhanced basal rate of aminoisobutyrate uptake, and are insulin resistant with regard to maximal insulin-stimulated uptake of aminoisobutyrate at 0.1mm-aminoisobutyrate. Because of the decreased maximal response to insulin, the concentration of insulin that elicits a half-maximal response of aminoisobutyrate uptake is decreased. Hepatocytes from diabetic animals, like those from starved rats, have significantly greater basal rates of aminoisobutyrate uptake; whereas the maximal absolute insulin response is the same as control cells, the percentage response is smaller. These cells bind significantly more insulin than do control cells. The increase in insulin binding is reflected in a shift to the left of the dose-response curve for insulin-stimulated uptake of aminoisobutyrate. These studies indicate that there is no insulin resistance with regard to uptake of aminoisobutyrate in hepatocytes from older obese rats. Furthermore, the insulin resistance observed in hepatocytes from starved rats occurs despite an increase in the number of receptors per unit surface area and cannot be explained by alterations in the interaction between insulin and its receptor. The enhanced insulin binding per unit surface area, however, is reflected in the shift to the left of the dose-response curve for insulin. This is also true for hepatocytes from diabetic animals, in which insulin binding per cell is increased.

Age Factors↗
PubMed1996

Dependence of adaptative regulation for IL-1 beta action on system A activity in human synovial cells.

Human synovial cells are a suitable model for estimating the physiopathological effects of IL-1 beta (IL-1) in joint. Given the importance of this cytokine in the modulation of cell metabolic activities, we set out to study the action of IL-1 on the neutral amino acid transport A system, using the methyl (aminoisobutyric) acid (MeAIB), the most highly specific and nonmetabolizable substrate for the A system. Stimulation of system A activity by adaptative regulation is a prerequisite to obtain an increase of MeAIB uptake in IL-1-treated cells, since cells which had been grown in a normal medium did not express stimulation of system A activity when IL-1 was added. The IL-1-mediated MeAIB uptake is independent of protein synthesis, since cycloheximide (CHX) did not inhibit MeAIB uptake, and characterized by a decrease in the Michaelis constant K(m) (0.147 vs. 0.270 mmol/l, IL-1 vs. control) and a slight increase in maximal velocity (Vmax) (4.59 vs. 3.89 nmol/mg prot/10 min, IL-1 vs. control). These observations indicate that IL-1 induces modifications in both system A transporter affinity and number. Moreover, we indicate that system A should be responsive in vivo to IL-1 in the same way since derepression and IL-1 action occurred in the presence of human synovial fluid.

Amino Acids↗
PubMed1996

Regulatory volume increase in rat lacrimal gland acinar cells.

The volume of acinar cells isolated from rat lacrimal glands was measured during hypertonic shock. Cells shrank in hypertonic solutions, but a regulatory volume increase (RVI) was only observed under certain conditions. In HEPES-buffered solutions at 37 degrees C, an RVI was observed. This was inhibited by 20 microM bumetanide, an inhibitor of Na(+)-K(+)-2Cl- cotransport. RVI did not occur in HEPES-buffered solutions at 20 degrees C suggesting that Na(+)-K(+)-2Cl- cotransport is inactive at this temperature. In HCO3- buffered solutions however, an RVI was observed at 20 degrees C. In these conditions, the RVI was inhibited by 500 microM 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonic acid (H2-DIDS) and 10 microM 5-(N-methyl-N-isobutyl)-amiloride (MIBA) indicating the involvement of Cl(-)-HCO3- exchange and Na(+) -H+ exchange respectively. RVI was also supported by a mixture of neutral amino acids, and by the nonmetabolizable amino acids 5 mM alpha-(methylamino)isobutyric acid (MeAIB) and 5 mM alpha-aminoisobutyric acid (AIB). These data suggest that the accumulation of amino acids, possibly by the system A Na(+)-coupled amino acid cotransporter, contributes to RVI in these cells. In conclusion, rat lacrimal gland acinar cells are capable of undergoing RVI following shrinkage by hypertonic shock.

Amino Acids↗