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K Unsicker

Publications and source records attributed to K Unsicker.

At least 91 records · Page 5Linked to original sources
PubMed1996

The survival response of mesencephalic dopaminergic neurons to the neurotrophins BDNF and NT-4 requires priming with serum: comparison with members of the TGF-beta superfamily and characterization of the serum-free culture system.

The neurotrophins, brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4), are established survival promoting molecules for dopaminergic (DAergic) neurons cultured from the fetal rat midbrain floor. We have cultured and compared the survival of embryonic day (E) 14 mesencephalic cells in fully defined, serum-free medium, with serum-primed cultures (one hour during dissociation). Cultures were characterized using antibodies against neuron-specific enolase (NSE), tyrosine hydroxylase (TH), vimentin, glial fibrillary acidic protein (GFAP), and the antigen A2B5. The absolute absence of serum did not reduce the survival of TH-positive DAergic neurons nor alter the percentages of cells staining for the above markers. Transforming growth factor-beta 3 (TGF-beta 3) and glial cell line-derived neurotrophic factor (GDNF), two members of the TGF-beta superfamily, both promoted the survival of TH-positive cells (TGF-beta 3: 2-fold; GDNF: 1.6-fold) over the 8-day culture period. Survival mediated by TGF-beta 3 and GDNF was independent of whether or not the cells had been initially exposed to serum. In contrast, the survival promoting effects of BDNF and NT-4 were crucially dependent on serum priming. RT-PCR for the full-length trkB high affinity neurotrophin receptor revealed its presence in both culture systems. We conclude that priming with serum is important to make DAergic neurons fully responsive to BDNF and NT-4. Underlying mechanisms might be sought at the level or distal of trkB receptor expression, without excluding the possiblity that serum elicits production of growth factors that synergistically act with neurotrophins in these cultures.

Animals↗
PubMed1996

Distinct modulatory actions of TGF-beta and LIF on neurotrophin-mediated survival of developing sensory neurons.

The neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) are important for the regulation of survival and differentiation of distinct, largely non-overlapping populations of embryonic sensory neurons. We show here that the multifunctional cytokine transforming growth factor-beta (TGF-beta) fails to maintain sensory neurons cultured from embryonic day (E) 8 chick dorsal root ganglia (DRG), although DRG neurons are immunoreactive for the TGF-beta receptor type II, which is essential for TGF-beta signaling. However, in combination with various concentrations of NT-3 and NT-4, but not NGF, TGF-beta 3 causes a further significant increase in neuron survival. In DRG cell cultures treated with NGF, NT-3, and NT-4, a neutralizing antibody to TGF-beta decreases neuron survival suggesting that endogenous TGF-beta in these cultures affects the efficacies of neurotrophins. Consistent with this notion and a modulatory role of TGF-beta in neurotrophin functions is the observation that TGF-beta 2 and -beta 3 immunoreactivities and TGF-beta 3 mRNA are located in embryonic chick DRG in close association with neurons from E5 onwards. We also show that leukemia inhibitory factor (LIF) significantly decreases NGF-mediated DRG neuron survival. Together, these data indicate that actions and efficacies of neurotrophins are under distinct control by TGF-beta and LIF in vitro, and possibly also in vivo.

Animals↗
PubMed1996

Expression and localization of GDNF in developing and adult adrenal chromaffin cells.

Glial cell line-derived neurotrophic factor (GDNF) is a widely distributed member of the transforming growth factor-beta superfamily and a potent neurotrophic molecule for several neuron populations in the peripheral and central nervous system. We show here that adrenal medullary chromaffin cells synthesize GDNF mRNA and contain immunoreactive GDNF protein. GDNF immunoreactivity can be found as early as embryonic day 16 in chromaffin progenitor cells of the rat adrenal gland and becomes more prominent with age. Most of the chromaffin cells within the adult rat adrenal medulla are GDNF immunoreactive, including both the noradrenergic and adrenergic subpopulations. The functions of adrenal medullary GDNF are still enigmatic but may include both auto/paracrine roles and retrograde trophic support of preganglionic neurons in the spinal cord or of sensory neurons that innervate chromaffin cells.

Adrenal Medulla↗
PubMed1996

A chromaffin cell-derived protein induces the NADPH-diaphorase phenotype in cultured rat spinal cord neurons.

We have recently demonstrated that neurotrophins induce reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity in cultured spinal cord neurons. One prominent neuron population of the spinal cord expressing NADPH-diaphorase activity in vivo are preganglionic sympathetic neurons, including those innervating the adrenal medulla. These neurons receive trophic support from their target. We have shown previously that chromaffin cells contain as yet unidentified neurotrophic molecules, which may include releasable factors relevant for the survival and differentiation of developing preganglionic sympathetic neurons. We have studied the influence of proteins derived from bovine chromaffin cells and released by nicotine on NADPH-diaphorase expression in spinal cord cultures established from 16-day-old rat embryos. At this embryonic age, NADPH-diaphorase activity becomes apparent in the spinal cord and predominantly expressed in sympathetic nuclei. Similar to brain-derived neurotrophic factor and neurotrophin-4, a heat- and trypsin-sensitive component from chromaffin cells contained in granule preparations up-regulated the number of NADPH-diaphorase-positive neurons in spinal cord cultures. Combined application of this activity and neurotrophin-4 resulted in an additive effect, indicating that the effect of the chromaffin cell-derived active component is not mediated by one of the trk B ligands. This was confirmed by co-treatment studies with the trk-signalling pathway inhibitor K252b, which did not inhibit the effect of the chromaffin cell-derived protein(s). Further studies revealed that NADPH-diaphorase reactivity is inducible in spinal cord neurons at any time point throughout the entire culture period of six days, suggesting de novo induction of the enzyme rather than a survival-promoting effect of the activity from chromaffin cells. Culture supernatants from nicotine-stimulated bovine chromaffin cells induced NADPH-diaphorase-positive neurons at the same magnitude as the material obtained from chromaffin granule preparations. Our data suggest that chromaffin cell-derived proteins are capable of up-regulating NADPH-diaphorase activity or to induce de novo this transmitter phenotype in neuron populations of the spinal cord, which may include preganglionic sympathetic neurons.

Animals↗
PubMed1996

TGF-beta rescues target-deprived preganglionic sympathetic neurons in the spinal cord.

Transforming growth factors beta (TGF-beta), a family of pleiotropic cytokines, are widely distributed in the developing and adult nervous system. In order to further determine the neural functions of TGF-beta, we have localized the TGF-beta isoforms 1, 2 and 3 in the adult rat adrenal medulla and studied the neuroprotective capacity of one representative family member, TGF-beta 2, for those spinal cord neurons which innervate adrenal chromaffin cells and which die after destruction of the adrenal medulla. Unilateral electrothermal destruction of the adrenal medulla led to the disappearance of 25% of sympathetic preganglionic neurons, which are located in the intermediolateral (IML) column of thoracic spinal cord segments 7-10 and can be selectively marked by NADPH-diaphorase. The neurons which disappeared following adrenomedullectomy constitute the full set of neurons that innervate the adrenal medulla. Implantation of gelfoam soaked with 0.5 micrograms TGF-beta 2 into the adrenal wound cavity rescued all spinal cord neurons in the IML ipsilaterally to the lesioned side. Cytochrome c was not effective. Injections of [125I]TGF-beta 2 into the adrenal medulla did not result in retrograde transport and subsequent labelling of spinal cord neurons, suggesting that TGF-beta may exert its neuroprotective actions by indirect mechanisms. TGF-beta applied to cultured adrenocortical cells did not overtly increase the amount of mRNA for fibroblast growth factor-2, an established trophic molecule for sympathetic preganglionic spinal cord neurons. The mechanisms by which TGF-beta exerts its neurotrophic effect are therefore unclear. Even so, our data provide the first evidence that TGF-beta may play an important role in vivo in the control of maintenance of a population of spinal cord neurons.

Adrenal Cortex↗
PubMed1995

Screening of interleukins for survival-promoting effects on cultured mesencephalic dopaminergic neurons from embryonic rat brain.

In order to evaluate the neurotrophic potential that interleukins may have for nigrostriatal dopaminergic neurons, we have applied the interleukins 1 alpha, 1 beta, and 2 through 12 to cultures of E14 rat midbrain floor cells enriched for dopaminergic neurons. IL-6 and -7 were the only interleukins that modestly (130%, as compared to controls, 100%) promoted survival of dopaminergic neurons visualized by their immunoreactivity for tyrosine hydroxylase over an 8-day culture period. The effect was not mediated by astroglial cells. We conclude that most interleukins per se may not act as neurotrophic factors for dopaminergic neurons, although several of them occur in the embryonic and adult CNS.

Animals↗
PubMed1995

Immunocytochemical localization of the heparin-binding growth-associated molecule (HB-GAM) in the developing and adult rat cerebellar cortex.

The heparin-binding, growth-associated molecule (HB-GAM) is a developmentally regulated protein that belongs to a new family of heparin-binding molecules, not related to the fibroblast growth factors (FGFs), with putative functions during cell growth and differentiation. In order to further study the functional role of HB-GAM we have used a polyclonal antiserum, raised against the purified protein to localize HB-GAM in the developing and adult rat cerebellar cortex. During postnatal development HB-GAM-like immunoreactivity (IR) was found to be present in all layers of the cerebellar cortex. IR was mainly associated with processes or extracellular structures but not with cell bodies. Throughout all the stages examined the molecular layer was clearly labeled, whereas staining in the internal granular layer was diffuse. IR in the external granular layer on postnatal day 1 and 8 was found to be associated with radially oriented fibres connecting the internal granular layer with the pial surface of the cerebellum. The intensity of this staining seemed to increase from day 1 to 8. Staining of corresponding areas with an antiserum against the glial fibrillary acidic protein (GFAP) suggested that the HB-GAM antiserum in the developing cerebellar cortex labels Bergmann glia fibres of Golgi epithelial cells. Because of the diffuse staining of the molecular layer in the adult rat it was not possible to distinguish whether radial fibres in the adult contained any HB-GAM IR. Golgi epithelial cells are considered as crucial for the migration of granular cells during the differentiation of the cerebellar cortex. We therefore speculate that the association of HB-GAM-like IR may be of functional relevance. The fact that molecules, such as tenascin, known to be involved in morphogenetic events show a similar spatiotemporal distribution pattern further underscores this hypothesis. HB-GAM, which possesses a classical signal sequence, might be release in the extracellular space and could mediate adhesion phenomena by binding to heparin-like molecules associated with the neuronal membrane. Therefore, it will be important to investigate whether specific antibodies against HB-GAM are able to interfere with normal cerebellar development in vitro and in vivo.

Animals↗
PubMed1995

Vasoactive intestinal peptide but not galanin promotes survival of neonatal rat sympathetic neurons and neurite outgrowth of PC12 cells.

The synthesis of the neuropeptide galanin (GAL) is greatly enhanced after axonal lesion in different neuron populations of the peripheral and central nervous system. In sympathetic ganglia, GAL-immunoreactive nerve fiber baskets have been found surrounding postganglionic neurons after axotomy. Until now, it is unclear if GAL may be involved in neuronal survival or regeneration as suggested for vasoactive intestinal peptide (VIP) that is also upregulated after nerve lesion. We have, therefore, studied the effects of GAL on survival of sympathetic neurons dissociated from newborn rat superior cervical ganglia and on neurite outgrowth of PC12 cells. These effects were compared to those elicited by VIP. Whereas VIP promoted survival of about 10% of sympathetic neurons 2 days after nerve growth factor deprivation and induced neurite outgrowth of PC12 cells already at 6 h after addition of the peptide, GAL had no effect in either of these culture systems. While the induction of VIP may be beneficial for axotomized neurons, the functional significance of increased GAL levels remains to be established.

Animals↗
PubMed1995

Expression of interleukin-6 (IL-6) and IL-6 receptor mRNAs in rat adrenal medulla.

Using in situ hybridization and reverse transcription combined with the polymerase chain reaction (RT-PCR) we have studied the expression and developmental regulation of interleukin-6 (IL-6) and its receptor mRNAs in rat adrenal medulla. Labeling for both transcripts was much more intense over the adrenal medulla than over cortical regions at postnatal day 70. Levels of mRNAs of both genes measured by RT-PCR increased from birth to adulthood. In vitro survival and neurite growth of chromaffin cells from early postnatal rats were not affected by IL-6. Even so, the presence and developmental regulation of IL-6 and its receptor are consistent with a possible auto- or paracrine role of IL-6 in rat adrenal medulla.

Adrenal Glands↗
PubMed1995

Targeted disruption of the glucocorticoid receptor gene blocks adrenergic chromaffin cell development and severely retards lung maturation.

The role of the glucocorticoid receptor (GR) in glucocorticoid physiology and during development was investigated by generation of GR-deficient mice by gene targeting. GR -/- mice die within a few hours after birth because of respiratory failure. The lungs at birth are severely atelectatic, and development is impaired from day 15.5 p.c. Newborn livers have a reduced capacity to activate genes for key gluconeogenic enzymes. Feedback regulation via the hypothalamic-pituitary-adrenal axis is severely impaired resulting in elevated levels of plasma adrenocorticotrophic hormone (15-fold) and plasma corticosterone (2.5-fold). Accordingly, adrenal glands are enlarged because of hypertrophy of the cortex, resulting in increased expression of key cortical steroid biosynthetic enzymes, such as side-chain cleavage enzyme, steroid 11 beta-hydroxylase, and aldosterone synthase. Adrenal glands lack a central medulla and synthesize no adrenaline. They contain no adrenergic chromaffin cells and only scattered noradrenergic chromaffin cells even when analyzed from the earliest stages of medulla development. These results suggest that the adrenal medulla may be formed from two different cell populations: adrenergic-specific cells that require glucocorticoids for proliferation and/or survival, and a smaller noradrenergic population that differentiates normally in the absence of glucocorticoid signaling.

Adrenal Cortex↗
PubMed1995

Heterogeneity of human neuroblastoma cell lines in their proliferative responses to basic FGF, NGF, and EGF: correlation with expression of growth factors and growth factor receptors.

Growth factors can induce both proliferation or differentiation of neuroblastoma (NB) cells through interaction with specific receptors. Using two automated colorimetric assays for determinations of cell numbers, the present study demonstrates that a) different NB and neuroepithelioma cell lines show distinct responses, both qualitatively and quantitatively, to basic FGF (bFGF), NGF, and EGF; b) even closely related NB cell lines (e.g., SK-N-SH, SH-SY5Y, and SHEP) do not respond uniformly to these factors; c) responses of the two neuroepithelioma cell lines employed (SK-N-MC and CHP-100) differ, but match those of certain NB cell lines; and d) two growth factors, bFGF and EGF, may both stimulate or inhibit proliferation, depending on the cell line studied. Specifically, IMR-32, SK-N-SH, and SH-SY5Y showed a mitogenic response to each growth factor. Maximal proliferative responses ranged from 204-355% as compared to controls (100%). GICAN was stimulated by NGF (199%), and SK-N-MC and NMB by EGF (282 and 140%, respectively), but other factors were ineffective. CHP-100 and GIMEN were inhibited by bFGF. NGF and EGF were not effective on CHP-100 cells, while EGF caused an arrest of mitogenic activity in GIMEN cells, and NGF stimulated their proliferation. Cell lines SHEP and LAN1 did not respond to any factor. To begin to analyze putative relationships of growth factor responsiveness and growth factor/growth factor receptor expressions, IMR-32, GIMEN, and LAN1 cell lines were studied for the presence of bFGF, NGF, FGF receptors (R)-1 (flg) and FGFR-4, trk, and low-affinity NGF receptor (p75) mRNAs.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Division↗
PubMed1995

Fibroblast growth factor-2-like immunoreactivity in auditory brainstem nuclei of the developing and adult rat: correlation with onset and loss of hearing.

Fibroblast growth factor-2 (FGF-2; basic FGF) is widely distributed in the developing and adult brain and has numerous effects on cultured and lesioned neural cells. The physiological role of FGF-2 in the unlesioned nervous system, however, is still not understood. We have studied the distribution of FGF-2 in the developing, adult, and functionally impaired central auditory system of the rat using specific antibodies and peroxidase-antiperoxidase immunocytochemistry. FGF-2-like immunoreactivity (FGF-2-IR) occurred in neuronal cell bodies and/or nerve fibers but was very rarely observed in glial cells. Several auditory brainstem nuclei, including the superior paraolivary nucleus, the medial superior olive, the lateral and ventral trapezoid nuclei, and the central nucleus, as well as the external cortex of the inferior colliculus, were entirely devoid of FGF-2-IR. In the dorsal cochlear nucleus, the lateral superior olive, and the nuclei of the lateral lemniscus, FGF-2-IR was not detectable in nerve cell bodies prior to adult age. Neurons in the medial geniculate body exhibited FGF-2-IR only transiently, from postnatal day (P) 5 until P16. Neurons in the medial nucleus of the trapezoid body were immunoreactive from P8 onwards. FGF-2-IR in anteroventral and posteroventral cochlear neurons disappeared at P14, i.e., at the onset of hearing, but immunoreactivity returned after P21. A transient expression of FGF-2 around the time when hearing function commences was observed in the dorsal cortex of the inferior colliculus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

TGF-beta superfamily members promote survival of midbrain dopaminergic neurons and protect them against MPP+ toxicity.

The superfamily of transforming growth factors-beta (TGF-beta) comprises an expanding list of multifunctional proteins serving as regulators of cell proliferation and differentiation. Prominent members of this family include the TGF-beta s 1-5, activins, bone morphogenetic proteins and a recently discovered glial cell line-derived neurotrophic factor (GDNF). In the present study we demonstrate and compare the survival promoting and neuroprotective effects of TGF-beta 1, -2 and -3, activin A and GDNF for midbrain dopaminergic neurons in vitro. All proteins increase the survival of tyrosine hydroxylase-immunoreactive dopaminergic neurons isolated from the embryonic day (E) 14 rat mesencephalon floor to varying extents (TGF-beta s 2.5-fold, activin A and GDNF 1.6-fold). TGF-beta s, activin A and GDNF did not augment numbers of very rarely observed astroglial cells visualized by using antibodies to glial fibrillary acidic protein and had no effect on cell proliferation monitored by incorporation of BrdU. TGF-beta 1 and activin A protected dopaminergic neurons against N-methyl-4-phenylpiridinium ion toxicity. Reverse transcription-polymerase chain reaction (RT-PCR) analysis indicated that TGF-beta 2 mRNA, but not GDNF mRNA, is expressed in the E14 rat midbrain floor and in mesencephalic cultures. We conclude that TGF-beta s 1-3, activin A and GDNF share a neurotrophic capacity for developing dopaminergic neurons, which is not mediated by astroglial cells and not accompanied by an increase in cell proliferation.

1-Methyl-4-phenylpyridinium↗
PubMed1995

Trophic and protective effects of growth/differentiation factor 5, a member of the transforming growth factor-beta superfamily, on midbrain dopaminergic neurons.

Growth/differentiation factor 5 (GDF5) is a novel member of the transforming growth factor-beta (TGF-beta) superfamily of multifunctional cytokines. We show here that GDF5 is expresed in the developing CNS including the mesencephalon and acts as a neurotrophic, survival promoting molecule for rat dopaminergic midbrain neurons, which degenerate in Parkinson's disease. Recombinant human GDF5 supports dopaminergic neurons, dissected at embryonic day (E) 14 and cultured for 8 days under serum-free conditions, to almost the same extent as TGF-beta 3, and is as effective as glial cell line-derived neurotrophic factor (GDNF), two established trophic factors for midbrain dopaminergic neurons. In contrast to TGF-beta and GDNF, GDF5 augments numbers of astroglial cells in the cultures, suggesting that it may act indirectly and through pathways different from those triggered by TGF-beta and GDNF. GDF5 also protects dopaminergic neurons against the toxicity of N-methylpyridinium ion (MPP+), which selectively damages dopaminergic neurons through mechanisms currently debated in the etiology of Parkinson's disease (PD). GDF5 may therefore now be tested in animal models of PD and might become useful in the treatment of PD.

1-Methyl-4-phenylpyridinium↗
PubMed1995

Sympathoadrenal progenitors in embryonic chick sympathetic ganglia show distinct responses to glucocorticoid hormones.

The sympathoadrenal cell lineage originates from the neural crest and comprises the neurons of sympathetic ganglia, adrenal and extra-adrenal chromaffin cells, and the so-called small intensely fluorescent cells. In vitro studies using mammalian immature chromaffin cells, adrenal or sympathetic ganglionic progenitors, or ganglionic small intensely fluorescent cells, have suggested that glucocorticoid hormones are essential for inhibiting neuronal differentiation of sympathoadrenal progenitors and promoting the chromaffin cell phenotype. In avian systems, however, the distinct cellular phenotypes in this lineage and the molecular cues underlying their differentiation have not been fully explored. In the chick embryo, early sympathetic ganglion anlagen are populated by granule-containing cells that morphologically resemble small intensely fluorescent cells and chromaffin cell progenitors. These cells subsequently disappear from the ganglia, by death and by transition into fully differentiated sympathetic neurons, as indicated by the appearance of cells that are ultrastructurally intermediate between granule-containing cells and fully differentiated neurons (granule-containing cells in transition). In the present study, we show that treatment of cultured sympathetic cells dissociated from embryonic day (E) 7, 9, or 11 lumbar sympathetic ganglia with the glucocorticoid hormones hydrocortisone or corticosterone has neither an inhibitory nor an inductive effect on phenotypes of granule-containing cells or granule-containing cells in transition. In cell cultures of E15 ganglia, however, glucocorticoid treatment induces a granule-containing cell resembling the granule-containing phenotype. These results suggest that the early granule-containing cells and granule-containing cells in transition in chick sympathetic ganglia are not the counterparts of glucocorticoid-responsive mammalian small intensely fluorescent or chromaffin progenitor cells, despite their morphological similarity. However, E15 sympathetic ganglia apparently contain a glucocorticoid-responsive progenitor population that can differentiate into chromaffin-like cells. These progenitors seem to require a systemic or intraganglionic developmental signal or undergo a temporal switch that renders them susceptible to glucocorticoids.

Adrenal Medulla↗
PubMed1995

The neurotrophins BDNF, NT-3 and -4, but not NGF, TGF-beta 1 and GDNF, increase the number of NADPH-diaphorase-reactive neurons in rat spinal cord cultures.

Neurotrophins have multiple functions for the development of the nervous system. They can promote survival and differentiation of select neuronal populations, but have also been shown to play instructive roles in the determination of the transmitter phenotype of neurons. We have investigated the influence of neurotrophins on the expression of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), a histochemical marker for nitric oxide synthase, in spinal cord cultures established from 16-day-old rat embryos. At this embryonic age we found NADPH-d reactivity becoming apparent in the spinal cord and predominantly expressed in preganglionic autonomic nuclei. Numbers of NADPH-d-positive neurons in spinal cord cultures were very low 24 h after plating. They did not change significantly until day 4 in vitro. However, treatment with the neurotrophins BDNF, NT-3 or NT-4 significantly increased their numbers. The effect became apparent after just 24 h, and was significant with concentrations as low as 1 ng/ml. Treatment with BDNF, NT-3 and NT-4 also augmented numbers of NADPH-d-positive neurons when initiated after three or five days in culture, and became consistently apparent within 24 h. This suggests that the neurotrophin-mediated increase in NADPH-d-positive neurons is unlikely to be due to promotion of neuron survival. NGF and two members of the transforming growth factor-beta superfamily, which have pronounced trophic effects on select neuron populations in vitro, TGF-beta 1 and GDNF, were not effective. Combined application of NT-4 and NT-3 had no additive effect. Our data therefore suggest that neurotrophins are involved in the developmental regulation of NADPH-d activity in neuron populations of the spinal cord. Neuron populations affected may include preganglionic autonomic neurons. NADPH-d activity may be induced in neurons expressing the enzyme constitutively, yet at undetectable levels, or may be induced de novo.

Animals↗
PubMed1995

Localization of basic fibroblast growth factor in bovine adrenal chromaffin cells.

We have investigated basic fibroblast growth factor (FGF-2) localization in and release from isolated bovine adrenal chromaffin cells. In contrast to previous reports, we found no evidence of fibroblast growth factor (FGF) storage in catecholamine-containing chromaffin granules. Subcellular fractionation studies did not show enrichment of FGF-2 immunoreactivity in granules, and cholinergic stimulation failed to release FGF-2 into the medium. Our results suggest that adrenal chromaffin cells resemble other FGF-2-synthesizing cell types with respect to FGF storage and secretion.

Adrenal Medulla↗