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Calbindin D-28K and NADPH-diaphorase activity are localized in different populations of periglomerular cells in the rat olfactory bulb.

Calbindin D-28k (CaBP) immunocytochemistry and NADPH-diaphorase (ND) histochemistry have been combined in the rat olfactory bulb by successive incubations of the same sections. The outer strata showed a similar neuronal staining pattern for both markers with positive periglomerular neurons (although the CaBP-stained periglomerular cells were six-fold more abundant than the ND-active ones) and larger neurons scattered in the glomerular and external plexiform layers. Both populations of periglomerular cells were distinct but they did not show specific morphological characteristics nor a predominant distribution around ND-positive and negative glomeruli. The colocalization study demonstrates that the larger ND and CaBP-stained juxtaglomerular cells, identified according to their size, location and processes branching patterns as two types of short axon cells (superficial short-axon and Van Gehuchten Cells) were also independent populations.

Animals↗
PubMed1995

Contrasting effects of tamoxifen and ICI 182 780 on estrogen-induced calbindin-D 9k gene expression in the uterus and in primary culture of myometrial cells.

Antiestrogens have a large range of tissue- and promoter-specific actions, many of which still remain unclear, particularly in the uterus. Thus, we have analyzed the effects of two antiestrogens, tamoxifen (TAM) and ICI 182 780 (ICI) on the uterine estrogen-responsive gene calbindin-D9k (CaBP9k), in the ovariectomized rat uterus, and in primary cultures of myometrial cells. In the ovariectomized rat uterus, estradiol (E2) or E2 plus TAM induced CaBP9k mRNA to the same levels in 6h. Rats given TAM alone had the same mRNA concentration, but maximal induction was obtained later, 12h after injection. ICI alone did not induce CaBP9k gene expression. Rats given E2 plus ICI had low uterine CaBP9k mRNA levels at 6-12h that became undetectable at 24h. Thus ICI has a full antagonistic effect on E2-induced CaBP9k gene. Estradiol receptor (ER) assays showed that TAM had a partial antagonist effect, while ICI had a full antagonist effect on the ER. We also analyzed the effect of TAM and ICI on CaBP9k gene expression in primary cultures of myometrial cells. The effects were similar to those observed in whole uterus. Thus, TAM has mixed effects, being an agonist for CaBP9k gene induction, and an antagonist for ER. ICI antagonizes the effects of E2 on the CaBP9k gene in myometrial cells and in the intact uterus, but in a way that does not involve a decrease in the cellular content of ER. Instead, it interferes with at least one of the events leading to transcriptional activation.

Animals↗
PubMed2004

Spatial analysis reveals alterations of parvalbumin- and calbindin-positive local circuit neurons in the cerebral cortex of mutant mdx mice.

The aim of the present study was to investigate the spatial organization of selected populations of local circuit neurons in the cerebral cortex of the mutant mdx mouse, an acknowledged model of Duchenne Muscular Dystrophy. To this purpose, we quantified and compared the distribution of parvalbumin- and calbindin-positive neurons in the motor, somatosensory, visual, and anterior cingulate cortices of wild-type and mdx mice. The methodological approach was based on generation of two-dimensional Voronoi polygons from digital charts of the cell populations visualized immunohistochemically. Polygon areas were then analyzed and the derived coefficients of variation were statistically compared. Using this strategy, we were able to reveal, in mdx mice, changes involving both the above populations of interneurons. These changes were evident in the motor and anterior cingulate cortices but not in the somatosensory and visual cortices. In addition, the changes of coefficients of variation were area-specific in the cortex of mdx mice. The values increased in the motor cortex and decreased in the anterior cingulate cortex with respect to the corresponding values of wild-type animals. The present findings point out widespread alterations in the mdx cortex involving also areas not primarily related to sensorimotor integration. In addition, we demonstrate that cortical alterations of the local circuit machinery are characterized in mdx mice by individual regional differences.

Animals↗
PubMed2005

Calbindin D-28k is expressed in the microvascular basal lamina in the ventral horn at early time after transient spinal cord ischemia in the rabbit.

Much evidence has been accumulated that the increased expression of calbindin D-28k (CB) is involved in the blockade of calcium-evoked excitotoxicity in cerebral ischemia. We investigated the expression of CB in the basal lamina of microvessels in the ventral horn of the rabbit spinal cord after transient spinal cord ischemia. Spinal cord sections at the level of L7 were immunostained using monoclonal antibody raised against CB at light and electron microscopic levels. CB immunoreactivity was detected in the basal lamina of microvessels at 30 min after ischemic insult. By 3 h after ischemia, CB immunoreactivity was increased in the basal lamina of the microvessels. CB immunoreactivity began to decrease at 6 h after ischemia and nearly disappeared at 48 h after ischemic insult. For calcium detection in the blood vessels of spinal cord, we conducted an alizarin red staining. Alizarin red reactivity was detected in some microvessels at 3 h after ischemic insult. Our results suggest that the ectopic expression of CB in the microvascular basal laminae may be associated with the buffering of calcium in the endothelial cells of microvessels after ischemic damage.

Animals↗
PubMed2006

Distribution of calbindin-28kD and parvalbumin in V1 in normal adult Cebus apella monkeys and in monkeys with retinal lesions.

Several proteins have their normal patterns of distributions altered by monocular visual deprivation. We studied the distribution of the calcium-binding proteins calbindin-28kD (Cb) and parvalbumin (Pv) in V1 in normal adult Cebus apella monkeys and in monkeys with monocular retinal lesions. In normal monkeys, the interblobs regions in layers 2/3 and the layer 4B are intensely labeled for Cb, while Pv reaction showed a complementary labeling pattern with a stronger staining in layers 4A, 4C and in the blob regions in layers 2/3. In monkeys with monocular retinal lesion, the laminar distribution of these proteins was differentially affected, although both reactions resulted in stronger labeling in non-deprived ocular dominance columns. While Cb reaction resulted in stronger labeling in layers 1 through 5, Pv labeling was heavier in layers 2/3, 4A and 4C. There was a clear reduction in the intensity of neuropil staining for both Pv and Cb in deprived ocular dominance columns with little or no reduction in number of labeled cells. This reduction could thus be attributed to activity-dependent changes at synapses level.

Animals↗
PubMed2005

Calbindin-D28k immunoreactivity in the spinal cord of Xenopus laevis and its participation in ascending and descending projections.

Immunohistochemistry for calbindin-D28k (CB) revealed that the spinal cord of Xenopus laevis possess a large number of CB-containing neurons widely distributed in both the dorsal and ventral horns, including areas which possess long ascending projections to supraspinal structures. In addition, the presence of CB-immunoreactive axons in the spinal funiculi suggested that descending projections containing this calcium binding protein may originate in different brainstem nuclei. Apart from mapping CB-containing elements in the spinal cord, a double labeling approach was used that combined the retrograde transport of dextran amines with CB immunohistochemistry. Thus, dextran amine injections into the lateral reticular region of the rhombencephalon, the parabrachial region, the mesencephalon and the dorsal thalamus revealed many retrogradely labeled cells in the spinal cord, a few number of which were double labeled for CB and found in the superficial dorsal horn and in the ventral medial region of the ventral horn. Their axons passed mainly via the lateral funiculus. Tracer application into the cervical spinal cord, combined with CB immunohistochemistry, resulted in retrogradely labeled cells throughout the brain, five groups of which showed CB immunoreactivity: (1) the mesencephalic trigeminal nucleus, (2) the laterodorsal tegmental nucleus, (3) the raphe nucleus, (4) the middle reticular nucleus and (5) the inferior reticular nucleus. The presence of CB in spinal pathways suggests that CB may play a role in controlling spinal cells, mainly subserving visceroceptive and nociceptive information to supraspinal levels, and might also modulate reticulospinal pathways.

Animals↗
PubMed2005

Simultaneous glutamate and GABA(A) receptor agonist administration increases calbindin levels and prevents hippocampal damage induced by either agent alone in a model of perinatal brain injury.

Perinatal brain injury is associated with the release of amino acids, principally glutamate and GABA, resulting in massive increases in intracellular calcium and eventual cell death. We have previously demonstrated that independent administration of kainic acid (KA), an AMPA/kainate receptor agonist, or muscimol, a GABA(A) receptor agonist, to newborn rats results in hippocampal damage [Hilton, G.D., Ndubuizu, A., and McCarthy, M.M., 2004. Neuroprotective effects of estradiol in newborn female rat hippocampus. Dev. Brain Res. 150, 191-198; Hilton, G. D., Nunez, J.L. and McCarthy, M.M., 2003. Sex differences in response to kainic acid and estradiol in the hippocampus of newborn rats. Neuroscience. 116, 383-391; Nunez, J.L. and McCarthy, M.M., 2003. Estradiol exacerbates hippocampal damage in a model of preterm infant brain injury. Endocrinology. 144, 2350-2359; Nunez, J.L., Alt, J.J. and McCarthy, M.M., 2003. A new model for prenatal brain damage. I. GABA(A) receptor activation induces cell death in developing rat hippocampus. Exp. Neurol. 181, 258-269]. We now report that KA or muscimol alone administered to immature hippocampal neurons in culture induces significant cell death as evidenced by TUNEL assay. Surprisingly, simultaneous administration of equimolar quantities of these two agonists blocks the effect of either one alone. Moreover, treatment of newborn pups results in less damage compared to either muscimol or KA alone. We further observed that immunoreactivity for the calcium-binding protein, calbindin D(28K), is increased in the brains of pups simultaneously administered KA and muscimol as compared to either alone.

Animals↗
PubMed2006

Calbindin D-28 and microtubule-associated protein-2: their use as sensitive immunohistochemical markers of cerebellar neurotoxicity in a regulatory toxicity study.

The aim of this study was to develop an immunohistochemical (IHC) method for calbindin D-28 (CB-28) and microtubule-associated protein-2 (MAP-2) and evaluate their expression as markers in the detection, characterisation and grading of unexpected cerebellar toxicity in the rat. High power examination of H&E-stained brain sections of treated rats 2 days following a single oral dose of a novel compound revealed irregular vacuolation of the molecular layer and Purkinje cell degeneration. Animals killed after 14 days recovery showed Purkinje cell degeneration but vacuolation of the molecular layer was absent. In control animals, CB-28 and MAP-2 expression was high in Purkinje cell dendrites and cell bodies in the molecular layer. In treated animals, low power examination revealed loss of CB-28 and MAP-2 expression in degenerating neurons arranged in parasagittal stripes within the vermis. This is the first description of successful use of these two markers in a regulatory toxicity study using FFPE brain. In particular, CB-28 provides a sensitive method for characterising CNS toxicity which can be detected at low power enabling easier detection, screening and grading of neurotoxicity.

Administration, Oral↗
PubMed2005

Visually-induced NGFI-A protein expression in the calbindin-, parvalbumin- and nitric oxide synthase-neuronal populations of the rat superior colliculus.

The expression of the immediate early gene NGFI-A in the nervous system is induced by sensory stimulation and seems to be related to long-term synaptic plasticity. We have used double-labeling immunohistochemistry to identify calbindin (CB)(+), parvalbumin (PV)(+) and neuronal nitric oxide synthase (nNOS)(+) neurons that also expressed the protein encoded by this immediate early gene after light-exposure on in the superficial layers of the rat superior colliculus (sSC). The majority of the NGFI-A(+) cells were not double-labeled for the tested markers. In the stratum zonale+stratum griseum superficiale (SZ/SGS), only 17.8%, 8.0% and 12.1% of NGFI-A(+) cells were also labeled for CB, PV or nNOS, respectively. In the stratum opticum (SO), only 10.5% of the NGFI-A(+) cells were also CB(+). Furthermore, only a small subset of each population expressed the NGFI-A protein after light-exposure. In the SZ/SGS, 35.7% of the CB(+), 32.1% of the PV(+) and 26.6% of the nNOS(+) neurons also expressed the NGFI-A. In the SO, 31.7% of the CB(+) neurons also expressed the NGFI-A. The proportional distribution of the nNOS(+)/NGFI-A(+) neurons throughout the SZ/SGS layers showed a slight but significant rostro-caudal gradient. No significant difference was observed for the other markers, indicating homogeneous activation of these populations throughout the retinotopic map. Our results suggest that the visually-driven NGFI-A expression is not restricted to a specific population of the sSC and that visual processing in this structure, as assessed by the expression of this candidate-plasticity protein, involves the activation of subsets of ascending and non-ascending projection neurons.

Animals↗
PubMed2005

Vitamin D receptor is required for dietary calcium-induced repression of calbindin-D9k expression in mice.

Calbindin (CaBP), the vitamin D-dependent calcium-binding protein, is believed to play an important role in intracellular calcium transport. The aim of this study was to investigate the effect of high dietary calcium on the expression of CaBP-D9k and CaBP-D28k in the presence and absence of a functional vitamin D receptor (VDR). Treatment with the HCa-Lac diet containing 2% calcium, 1.5% phosphorus and 20% lactose reversed the hypocalcemia seen in adult VDR-null mice in 3 weeks but did not significantly change the blood ionized calcium in wild-type mice. This dietary treatment dramatically suppressed both the duodenal and the renal CaBP-D9k expression in wild-type mice at both mRNA and protein levels but had little effect on the expression of the same gene in VDR-null mice. Removal of this diet gradually restored the expression of CaBP-D9k to the untreated level in wild-type mice. Only moderate or little change in CaBP-D28k expression was seen in wild-type and VDR-null mice fed with the HCa-Lac diet. The VDR content in the duodenum or kidney of wild-type mice was not altered by the dietary treatment. These results suggest that calcium regulates CaBP-D9k expression by modulating the circulating 1,25-dihydrxyvitamin D(3) level and that VDR is thus required for the dietary calcium-induced suppression of CaBP-D9k expression. Calcium regulation of the CaBP-D9k level may represent an important mechanism by which animals maintain their calcium balance.

Animals↗
PubMed2006

Assessment of calcium-binding proteins (Parvalbumin and Calbindin D-28K) and perineuronal nets in normal and scrapie-affected adult sheep brains.

Scrapie is a prion disease in small ruminants that manifests itself with neurological clinical signs amongst which are ataxia and tremors. These signs can be explained partially by an imbalance in central inhibitory innervation. The study of the brain's inhibitory neuronal GABAergic populations and of their extracellular matrix has been used to define, in part, the pathogenesis of human prion diseases and scrapie models in rodents. The brain's distribution of neuronal GABAergic subpopulations has been monitored carefully using, as markers, antibodies against the calcium binding proteins parvalbumin and calbindin D-28K. The distribution of this perineuronal net marker was evaluated by means of affinity histochemistry with W. floribunda agglutinin. These techniques were performed on the brains of nine scrapie-positive sheep and on four infection-free sheep. These animals had undergone previously a clinical follow-up as well as a lesion profile and an immunohistochemical profile of the scrapie-associated prion protein deposition in the brain. The study of calcium-binding proteins revealed an alteration of the parvalbumin positive GABAergic neuronal subpopulation. In scrapie-positive cases, a reduction in stained neuronal perykaria was observed, along with a marked reduction of neurite labelling. This finding was noticeable in regions such as the neocortex, particularly the motor frontal cortex, and was concomitant with a moderate PrPsc deposition and a mild degree of lesion. No changes were observed in the extracellular matrix study. The results of the present study provide a partial explanation for the mechanisms of scrapie clinical signs due to a disturbance of the parvalbumin-positive inhibitory neuronal population.

Animals↗
PubMed2004

Complex regulation of Calbindin-D(9k) in the mouse placenta and extra-embryonic membrane during mid- and late pregnancy.

Calbindin-D(9k) (CaBP-9k) is a cytosolic calcium-binding protein mainly expressed in the duodenum, uterus and placenta, however, the role of CaBP-9k in the regulation of fetal growth remains to be elucidated. The present study was performed to investigate the expression pattern and regulation of CaBP-9k by antagonists of steroid hormones related with steroid hormone receptors during mid- and late pregnancy in mouse placenta and extra-embryonic membrane. The expression level of CaBP-9k increased in the placenta, while it decreased in the extra-embryonic membrane during pregnancy. The mRNA expression levels of estrogen receptor alpha (ERalpha) and progesterone receptor (PR) appeared to increase in both placenta and extra-embryonic membrane during pregnancy, suggesting that the ER and PR mRNA and protein expressions of placental CaBP-9k are positively correlated, but expressions of extra-embryonic membrane CaBP-9k are reversely correlated with ERalpha and PR mRNA levels. In addition, the present study indicates that the expressions of CaBP-9k mRNA and protein are differentially up- or down-regulated by antagonists of estrogen (E2) and progesterone (P4) in mouse placenta and extra-embryonic membranes, which suggests that E2 and P4 may be dominant factors in the regulation of the CaBP-9k. In particular, RU486, an antagonist of P4, down-regulated the mRNA and protein levels of placental CaBP-9k, whereas it up-regulated the protein level of extra-embryonic membrane CaBP-9k. In conclusion, we demonstrated that the CaBP-9k is distinctly regulated in the mouse placenta and extra-embryonic membrane, probably via sex steroid hormones (E2 and P4) and their receptors through a complex pathway. Extended studies are needed to verify relevant factors to regulate CaBP-9k gene and to provide further insight into roles of CaBP-9k gene in these tissues for the control of reproductive functions.

Animals↗
PubMed2005

A calcium binding protein, calbindin-D9k, is mainly regulated by estrogen in the pituitary gland of rats during estrous cycle.

As a member of family of cytosolic calcium binding proteins, Calbindin-D9k (CaBP-9k) is expressed in female reproductive system and regulated by steroid hormones, estrogen (E2) and progesterone (P4), but its expression and role in pituitary gland have not been elucidated yet. Thus, in this study, we elucidated the expression of CaBP-9k mRNA and protein in pituitary gland of rats. During estrous cycle of rats, pituitary CaBP-9k level fluctuated, and its mRNA was highly elevated during an E2-dominant stage (proestrus and estrus), whereas its level disappeared at a P4-dominant stage (metestrus and diestrus). In parallel with CaBP-9k mRNA, an increased level of CaBP-9k protein was observed during proestrus and estrus, suggesting that pituitary CaBP-9k may be up-regulated by E2. In addition, spatial CaBP-9k expression was attested by immunohistochemistry. Pituitary CaBP-9k protein was localized in the cytoplasm of a specific cell type in the anterior lobe, and the positive cells were abundant at proestrus and estrus. The CaBP-9k-positive cells were mainly localized in the acidophils producing growth hormones and prolactin. To verify hormonal regulation of pituitary CaBP-9k in this tissue, immature rats were treated with a physiological dose of E2 in the absence or presence P4 for 3 days. In a time-dependent experiment, pituitary CaBP-9k protein was induced at 48 h after the final E2 injection. A significant increase in CaBP-9k protein was caused by E2, whereas P4 antagonized E2-stimulated CaBP-9k expression as similarly observed in the uterus. Taken together, these results indicated for the first time that pituitary CaBP-9k expression is regulated during estrous cycle, and its expression is mainly controlled by E2 and antagonized by P4, suggesting that pituitary CaBP-9k in female rats may be involved in the central function of the reproduction system.

Animals↗
PubMed2004

Expression and changes of calbindin D-28k immunoreactivity in the ventral horn after transient spinal cord ischemia in rabbits.

We examined ischemia-related changes of calbindin D-28k (CB) immunoreactivity in L(7) of the spinal ventral horn after transient spinal cord ischemia in rabbits. In the sham-operated group, CB immunoreactivity was not present in the spinal ventral horn, but CB immunoreactivity was detectable in the dorsal horn. CB immunoreactivity was detectable in the ventral horn at 30 min after ischemia: the CB immunoreactivity was found in glial cells identified as astrocytes. At 1 h after ischemia, CB immunoreactivity was highest and present at a few somata located in the lamina VII as well as many glial cells. CB immunoreactivity was lower in the lamina VII at 3 h after ischemia compared to 1 h post-ischemic group. By 2 days after ischemia, CB immunoreactivity was decreased in this region. In addition, the result of Western blot result showed the pattern of CB expression similar to that of immunohistochemistry. In conclusion, the ischemia-related changes of CB immunoreactivity in neurons and glial cells in the ischemic spinal ventral horn in rabbits may be related to modulation of intracellular calcium following transient ischemia.

Animals↗
PubMed2005

Quantitative assessment of developing afferent patterns in the cat inferior colliculus revealed with calbindin immunohistochemistry and tract tracing methods.

The central nucleus of the inferior colliculus (CNIC) is comprised of an orderly series of fibrodendritic layers. These layers include integrative circuitry for as many as 13 different ascending auditory pathways, each tonotopically ordered. Calcium-binding proteins, such as calbindin-D28k (CB), may be useful neurochemical markers for specific subsets of afferent input in these layers and their spatial organization that are developmentally regulated. In this study, CB-immunohistochemistry was used to examine 1-42 postnatal-day-old kitten and adult cat CNIC and anterograde tracers were used to label afferent projections from the lateral superior olivary nucleus (LSO) to the CNIC at similar ages. A distinct axonal plexus that is CB-immunopositive is described. This CB-afferent compartment is present at birth and persists throughout the ages examined. Already at birth, the CB-immunostained plexus in kitten CNIC is organized into discrete bands that are approximately 75 microm thick and 500 microm long. In adult CNIC, the periodic banded pattern of CB-immunostained fibers is similar to that in kittens albeit bands are thicker (145 microm) and longer (700 microm). Growth in band thickness in adult cat appears proportional to growth of the IC, whereas length of the dense CB-immunostained bands is somewhat more focused in the central region of fibrodendritic layers. The banded pattern of the CB-immunostained plexus is well correlated with the location and dimension of afferent projections from the LSO in newborn kitten labeled with carbocyanine dye, 1,1'-dioctodecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate and in adult cat labeled with wheat germ agglutinin conjugated with horseradish peroxidase. The results reveal a neurochemical marker for one type of synaptic compartment in CNIC layers, banding, that is organized before hearing onset in kittens, but that may undergo some postnatal pruning.

Afferent Pathways↗
PubMed2006

Deficiency in parvalbumin, but not in calbindin D-28k upregulates mitochondrial volume and decreases smooth endoplasmic reticulum surface selectively in a peripheral, subplasmalemmal region in the soma of Purkinje cells.

The Ca(2+)-binding proteins parvalbumin (PV) and calbindin D-28k (CB) are key players in the intracellular Ca(2+)-buffering in specific cells including neurons and have profound effects on spatiotemporal aspects of Ca(2+) transients. The previously observed increase in mitochondrial volume density in fast-twitch muscle of PV-/- mice is viewed as a specific compensation mechanism to maintain Ca(2+) homeostasis. Since cerebellar Purkinje cells (PC) are characterized by high expression levels of the Ca(2+) buffers PV and CB, the question was raised, whether homeostatic mechanisms are induced in PC lacking these buffers. Mitochondrial volume density, i.e. relative mitochondrial mass was increased by 40% in the soma of PV-/- PC. Upregulation of mitochondrial volume density was not homogenous throughout the soma, but was selectively restricted to a peripheral region of 1.5 microm width underneath the plasma membrane. Accompanied was a decreased surface of subplasmalemmal smooth endoplasmic reticulum (sPL-sER) in a shell of 0.5 microm thickness underneath the plasma membrane. These alterations were specific for the absence of the "slow-onset" buffer PV, since in CB-/- mice neither changes in peripheral mitochondria nor in sPL-sER were observed. This implicates that the morphological alterations are aimed to specifically substitute the function of the slow buffer PV. We propose a novel concept that homeostatic mechanisms of components involved in Ca(2+) homeostasis do not always occur at the level of similar or closely related molecules. Rather the cell attempts to restore spatiotemporal aspects of Ca(2+) signals prevailing in the undisturbed (wildtype) situation by subtly fine tuning existing components involved in the regulation of Ca(2+) fluxes.

Animals↗
PubMed2006

Anti-progestogenic effect of flutamide on uterine expression of calbindin-D9k mRNA and protein in immature mice.

A calcium binding protein, calbindin-D9k (CaBP-9k), is a cytosolic protein and regulated by steroid hormones in the reproductive tissues. Mouse CaBP-9k gene was predominantly regulated by progesterone (P4), whereas rat CaBP-9k was mainly regulated by 17beta-estradiol (E2) in the uterus. The induction of CaBP-9k can be employed as a biomarker for steroidal substrates as endocrine disruptors (EDs). Flutamide (FLU) is a non-steroidal anti-androgen or pro-drug that is rapidly metabolized to hydroxyflutamide, which may have both an anti-androgenic and anti-progestogenic activities. Thus, in the present study, we employed immature mice (14-day-old) subcutaneously injected with P4 (20 mg/kg/day) and/or FLU (5 mg/kg/day) for 3 consecutive days in the presence or absence of RU486, a pure PR antagonist (30 mg/kg/day), to analyze uterine CaBP-9k expression in this model. When immature mice were treated with P4, the expression levels of CaBP-9k mRNA and protein were significantly increased by P4. P4-induced expression levels of CaBP-9k mRNA and protein were abolished by FLU, in part, suggesting that FLU is a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mice. In addition, P4-induced CaBP-9k expression was completely reversed by RU486. Increased expression levels of CaBP-9k mRNA and protein were maintained for 24h after final injection with P4 in a time-dependent manner. However, CaBP-9k mRNA rapidly disappeared after 48 h and its protein level is similar with its mRNA. Treatment with FLU suppressed partially P4-induced CaBP-9k mRNA and protein until 24 h. Taken together, these results indicate that FLU has an anti-progestogenic activity and plays a role as a partial antagonist of P4 in the regulation of uterine CaBP-9k in immature mouse model.

Androgen Antagonists↗
PubMed1998

Cyclosporine A-induced decrease in calbindin-D 28 kDa in rat kidney but not in cerebral cortex and cerebellum.

Recently, we reported that in rat, cyclosporine A (CsA) markedly decreases the levels of calbindin-D (CABP-D) 28 kDa in kidney. CABP-D 28 kDa is a calcium-binding protein which is highly expressed in calcium-transporting tissues such as kidney or brain. In this study, we investigated whether, in addition to the kidney, CsA also has an effect on CABP-D 28 kDa in rat brain. Three groups of male Wistar rats received 15 mg/kg/day or 50 mg/kg/day of CsA orally for 12 days, whereas controls received vehicle solution for the same period. CABP-D 28-kDa protein and CsA were quantified in homogenates of kidney, cerebral cortex and cerebellum, and the localization of CABP-D 28 kDa was assessed in the different tissue sections by immunohistochemistry. In kidney, CABP-D 28 kDa was strongly and dose dependently decreased, and was located in tubular epithelial cells. In brain, CABP-D 28 kDa was not changed and was mainly located in pyramidal cells of the cortex and in cerebellum exclusively in Purkinje cells. High CsA concentrations were measured in kidney, more than 17-fold greater than those found in cortex. In cerebellum, CsA was below the limit of detection. These data suggest that at clinically relevant doses, CsA may not affect CABP-D 28-kDa levels in brain.

Animals↗