دورية أكاديمية

Glial growth factor rescues Schwann cells of mechanoreceptors from denervation-induced apoptosis.

التفاصيل البيبلوغرافية
العنوان: Glial growth factor rescues Schwann cells of mechanoreceptors from denervation-induced apoptosis.
المؤلفون: Kopp DM; Department of Zoology, University of Texas at Austin, Austin, Texas 78712, USA., Trachtenberg JT, Thompson WJ
المصدر: The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 1997 Sep 01; Vol. 17 (17), pp. 6697-706.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
اللغة: English
بيانات الدورية: Publisher: Society for Neuroscience Country of Publication: United States NLM ID: 8102140 Publication Model: Print Cited Medium: Print ISSN: 0270-6474 (Print) Linking ISSN: 02706474 NLM ISO Abbreviation: J Neurosci Subsets: MEDLINE
أسماء مطبوعة: Publication: Washington, DC : Society for Neuroscience
Original Publication: [Baltimore, Md.] : The Society, c1981-
مواضيع طبية MeSH: Denervation*, Apoptosis/*drug effects , Growth Inhibitors/*pharmacology , Mechanoreceptors/*drug effects , Nerve Tissue Proteins/*pharmacology , Schwann Cells/*drug effects, Animals ; Axons/metabolism ; Glia Maturation Factor ; Glycoproteins/metabolism ; Immunohistochemistry ; Mechanoreceptors/physiology ; Neuregulins ; Rats ; Rats, Wistar ; Receptor, ErbB-2 ; Receptors, Nerve Growth Factor/metabolism ; Schwann Cells/metabolism ; Schwann Cells/physiology
مستخلص: Golgi tendon organs and Pacinian corpuscles are peripheral mechanoreceptors that disappear after denervation during a critical period in early postnatal development. Even if regeneration is allowed to occur, Golgi tendon organs do not reform, and the reformation of Pacinian corpuscles is greatly impaired. The sensory nerve terminals of both types of mechanoreceptors are closely associated with Schwann cells. Here we investigate the changes in the Schwann cells found in Golgi tendon organs and Pacinian corpuscles after nerve resection in the early neonatal period. We report that denervation induces the apoptotic death of these Schwann cells and that this apoptosis can be prevented by administration of a soluble form of neuregulin, glial growth factor 2. Schwann cells associated with these mechanoreceptors are immunoreactive for the neuregulin receptors erbB2, erbB3, and erbB4, and the sensory nerve terminals are immunoreactive for neuregulin. Our results suggest that Schwann cells in developing sensory end organs are trophically dependent on sensory axon terminals and that an axon-derived neuregulin mediates this trophic interaction. The denervation-induced death of mechanoreceptor Schwann cells is correlated with deficiencies in the re-establishment of these sensory end organs by regenerating axons.
References: Hokkaido Igaku Zasshi. 1995 Jan;70(1):159-73. (PMID: 7744364)
Cell Tissue Res. 1982;224(3):673-83. (PMID: 7116419)
J Neurocytol. 1977 Apr;6(2):171-94. (PMID: 853311)
Brain Res. 1980 Apr 7;187(1):97-111. (PMID: 7357479)
Proc Natl Acad Sci U S A. 1993 Mar 1;90(5):1746-50. (PMID: 8383326)
J Histochem Cytochem. 1996 Nov;44(11):1331-5. (PMID: 8918908)
J Biol Chem. 1995 Jun 16;270(24):14523-32. (PMID: 7782315)
Physiol Bohemoslov. 1978;27(5):437-43. (PMID: 153537)
Cell. 1993 Mar 12;72(5):801-15. (PMID: 8453670)
Neuron. 1996 Mar;16(3):515-27. (PMID: 8785049)
Neuron. 1995 Sep;15(3):585-96. (PMID: 7546738)
J Neurosci. 1995 Feb;15(2):1329-40. (PMID: 7869101)
J Neurosci. 1988 May;8(5):1625-31. (PMID: 3130468)
Physiol Rev. 1992 Jul;72(3):623-66. (PMID: 1626033)
Neurosci Lett. 1992 Mar 30;137(2):237-40. (PMID: 1584466)
Cell. 1992 May 1;69(3):559-72. (PMID: 1349853)
Trends Neurosci. 1996 Jul;19(7):280-5. (PMID: 8799973)
Neuroscience. 1981;6(8):1675-86. (PMID: 7266885)
Nature. 1996 Jan 11;379(6561):174-7. (PMID: 8538769)
Biol Rev Camb Philos Soc. 1992 Aug;67(3):287-319. (PMID: 1420728)
Science. 1992 May 22;256(5060):1205-10. (PMID: 1350381)
Cell. 1994 Jul 15;78(1):5-8. (PMID: 8033211)
Curr Opin Neurobiol. 1993 Oct;3(5):683-93. (PMID: 8260817)
Prog Brain Res. 1964;13:175-213. (PMID: 14302958)
Physiol Bohemoslov. 1963;12:277-90. (PMID: 14060613)
Cell Mol Biol. 1990;36(4):415-20. (PMID: 2279265)
Proc Natl Acad Sci U S A. 1989 Dec;86(23):9193-7. (PMID: 2687875)
Acta Anat (Basel). 1990;137(3):278-81. (PMID: 2349873)
J Pathol. 1987 Dec;153(4):313-6. (PMID: 3323435)
J Neurocytol. 1978 Feb;7(1):71-91. (PMID: 632855)
Nature. 1993 Mar 25;362(6418):312-8. (PMID: 8096067)
Neurosci Res. 1987 Oct;5(1):1-15. (PMID: 3323953)
Neuron. 1995 Jan;14(1):133-41. (PMID: 7826631)
J Neurocytol. 1973 Jun;2(2):217-35. (PMID: 4775768)
Neurosci Lett. 1982 Aug 16;31(2):117-21. (PMID: 6813774)
Nature. 1986 Jan 16-22;319(6050):226-30. (PMID: 3945311)
Br J Cancer. 1972 Aug;26(4):239-57. (PMID: 4561027)
Mol Cell Neurosci. 1996 Apr;7(4):247-62. (PMID: 8793861)
J Neurosci. 1996 Oct 1;16(19):6107-18. (PMID: 8815893)
Cell. 1994 May 20;77(4):503-12. (PMID: 7514502)
J Neurocytol. 1992 Jan;21(1):50-66. (PMID: 1346630)
Prog Brain Res. 1976;43:59-64. (PMID: 130653)
Neuron. 1995 Jan;14(1):125-32. (PMID: 7826630)
Proc Natl Acad Sci U S A. 1990 Jul;87(13):4905-9. (PMID: 2164210)
Biochem J. 1992 Sep 1;286 ( Pt 2):331-4. (PMID: 1530564)
J Cell Biol. 1997 Apr 7;137(1):211-20. (PMID: 9105049)
J Neurobiol. 1994 Aug;25(8):937-52. (PMID: 7525869)
J Neurosci. 1997 Mar 1;17(5):1642-59. (PMID: 9030624)
J Neurosci. 1983 Jan;3(1):117-23. (PMID: 6185653)
معلومات مُعتمدة: NS 20480 United States NS NINDS NIH HHS
المشرفين على المادة: 0 (Glia Maturation Factor)
0 (Glycoproteins)
0 (Growth Inhibitors)
0 (Nerve Tissue Proteins)
0 (Neuregulins)
0 (Receptors, Nerve Growth Factor)
EC 2.7.10.1 (Receptor, ErbB-2)
تواريخ الأحداث: Date Created: 19970901 Date Completed: 19970923 Latest Revision: 20191025
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC6573136
PMID: 9254682
قاعدة البيانات: MEDLINE