Stem cell factor is a neurotrophic factor for neural crest-derived chick sensory neurons

Carnahan, JF; Patel, M. S.; Miller, J.

doi:10.1523/jneurosci.14-03-01433.1994

Cited by 47 publications

(22 citation statements)

References 33 publications

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“…From E5 onwards, some cells in the dorsal area of the dorsal root ganglia (DRG) were c-kit positive (not shown). This is in agreement with the in vitro studies of Carnahan et al (1994) who found that the Steel factor has a survival effect on medio-dorsal DRG neurons. The mesenchyme of the branchial arches was also strongly labelled by the c-kit probe.…”

Section: E9supporting

confidence: 93%

Steel and c‐kit in the development of avian melanocytes: A study of normally pigmented birds and of the hyperpigmented mutant silky fowl

Lecoin

Lahav

Martin

et al. 1995

Developmental Dynamics

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We describe here the expression of c-kit and Steel (SZ) genes during the development of melanocytes in normally pigmented strains of chick and quail compared to unpigmented (White Leghorn) and hyperpigmented (Silky Fowl) strains of chickens. By using the quailkhick chimera system, we found that the neural crest cells, which migrate dorso-laterally in the subectodermal mesenchyme to give rise to the melanocytes, express c-kit as early as E4, that is about 2 days after they have left the neural primordium. The SZ gene is expressed from E4 onward in the epidermis but not at all in the dermis at any developmental stage. As feather buds develop, S Z mRNA becomes restricted to the apical region of the feather filaments. During formation of the barbs and barbules of the down feather, production of the Steel factor is restricted to the external epidermal cells of the barbules. The cell bodies of the c-kit-positive melanocytes are then located in the internal border of the epidermal ridges and extend their processes toward the source of the Steel factor. We propose that the spa-

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Section: E9supporting

confidence: 93%

Steel and c‐kit in the development of avian melanocytes: A study of normally pigmented birds and of the hyperpigmented mutant silky fowl

Lecoin

Lahav

Martin

et al. 1995

Developmental Dynamics

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“…It has been shown that SCF acts as a neurotrophic factor, supporting neuron survival during development of the peripheral nervous system. 28,29 …”

Section: Discussionmentioning

confidence: 99%

Brain Repair by Hematopoietic Growth Factors in a Rat Model of Stroke

Zhao

Singhal

Duan

et al. 2007

Stroke

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Background and Purpose— Stem cell factor (SCF) and granulocyte-colony stimulating factor (G-CSF) are essential growth factors in hematopoiesis. We determined whether receptors for SCF and G-CSF exist in the brain and whether exogenous SCF and G-CSF are beneficial to brain repair after brain ischemia. Methods— A well-established rat model of experimental stroke was used in this study. SCF, G-CSF, SCF+G-CSF, or saline was subcutaneously administered 3 hours to 7 days after brain ischemia. Bromodeoxyuridine was administered simultaneously. Sensorimotor function was evaluated with a limb placement test and foot fault test over time. Results— We observed that receptors for SCF and G-CSF were expressed in both neurogenic regions and neurons. SCF-treated rats showed the best functional restoration at 1 week that was maintained 4, 7, and 10 weeks after the final injection. G-CSF-induced functional recovery was limited and unstable. Interestingly, stable but delayed functional improvement was seen in SCF+G-CSF-treated rats. Infarction size was significantly reduced in all growth factor-treated rats. In addition, SCF and SCF+G-CSF enhanced neural progenitor cell proliferation in the subventricular zone bilaterally, whereas G-CSF and SCF+G-CSF treatment increased bromodeoxyuridine -positive cells in periinfarct areas. Conclusions— SCF and G-CSF are neuroprotective and beneficial to functional restoration when administered during the acute phase after brain ischemia, indicating hematopoietic growth factors play a role in brain repair.

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“…Application of granulation tissue, rich in ED1 ϩ and ED2 ϩ macrophages, enhances regeneration of peripheral nerves after a test crush lesion (Miyauchi et al, 1997), a responses that may involve IL-1, insofar as IL-1 stimulates the local synthesis of nerve growth factor (NGF) by infiltrating macrophages (Heumann, 1987). Many factors produced by lymphoid cells are neurotrophic, including interleukins other than IL-1 (Kashima et al, 1992;Mehler et al, 1993;Awatsuji et al, 1993;Araujo and Cotman, 1993;van Coelln et al, 1995), granulocyte-macrophage colony-stimulating factor (van Coelln et al, 1995;Kannan et al, 2000), transforming growth factor-␤ (TGF␤; Poulsen et al, 1994), stem cell factor (Carnahan et al, 1994), and leukemia inhibitor factor (Murphy et al1993). Recently, IL-12 and IL-3 also have been reported to stimulate sympathetic neurite growth in mouse sympathetic superior cervical ganglion neurons (Kannan et al, 2000;Lin et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Changes in the density and distribution of sympathetic nerves in spleens from Lewis rats with adjuvant‐induced arthritis suggest that an injury and sprouting response occurs

Lorton

Lubahn

Lindquist

et al. 2005

J of Comparative Neurology

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Previously we demonstrated reduced norepinephrine concentrations in spleens from Lewis rats with adjuvant-induced arthritis (AA), an animal model of rheumatoid arthritis. This study extends these findings, examining the anatomical localization and density of sympathetic nerves in the spleen with disease development. Noradrenergic (NA) innervation in spleens of Lewis rats was examined 28 days following adjuvant treatment to induce arthritis or vehicle for the adjuvant by using fluorescence histochemistry for catecholamines, with morphometric analysis and immunocytochemistry for tyrosine hydroxylase. In AA rats, sympathetic nerve density in the hilar regions, where NA nerves enter the spleen, was increased twofold over that observed in vehicle-treated rats. In contrast, there was a striking twofold decline in the density of NA nerves in splenic regions distal to the hilus in arthritic rats compared with nonarthritic rats. In both treatment groups, NA nerves distributed to central arterioles, white pulp regions, trabeculae, and capsule. However, NA nerve density was reduced in the white pulp but was increased in the red pulp in AA rats compared with non-AA rats. These findings indicate an injury/sprouting response with disease development whereby NA nerves die back in distal regions and undergo a compensatory sprouting response in the hilus. The redistribution of NA nerves from white pulp to red pulp suggests that these nerves signal activated immune cells localized in the red pulp in AA. Although the mechanisms of this redistribution of NA nerves into the red pulp are not known, it may be due to migration from white pulp to red pulp of target immune cells that provide trophic support for these nerves. The redistribution of NA nerves into the red pulp may be critical in modulating immune functions that contribute to the chronic inflammatory stages of arthritis.

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Stem cell factor is a neurotrophic factor for neural crest-derived chick sensory neurons

Cited by 47 publications

References 33 publications

Steel and c‐kit in the development of avian melanocytes: A study of normally pigmented birds and of the hyperpigmented mutant silky fowl

Steel and c‐kit in the development of avian melanocytes: A study of normally pigmented birds and of the hyperpigmented mutant silky fowl

Brain Repair by Hematopoietic Growth Factors in a Rat Model of Stroke

Changes in the density and distribution of sympathetic nerves in spleens from Lewis rats with adjuvant‐induced arthritis suggest that an injury and sprouting response occurs

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