THE EFFECTS OF INSULIN-LIKE GROWTH FACTOR-1 AND NERVE GROWTH FACTOR ON DENERVATED MUSCLE ATROPHY

2001 ◽  
Vol 05 (03) ◽  
pp. 193-203 ◽  
Author(s):  
Boonsin Buranapanitkit ◽  
Zhuqing Qu ◽  
Morey M. Moreland ◽  
Alan Geater ◽  
George Somogyi ◽  
...  
Keyword(s):  
Growth Factors ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Muscle Atrophy ◽  
Interstitial Fibrosis ◽  
Insulin Like Growth Factor ◽  
Denervated Muscle ◽  
Nerve Growth ◽  
Wet Weight ◽  
The Mean

The effects of growth factors on denervated muscle atrophy in mouse gastrocnemius muscle were studied by morphometric, physiologic and histologic methods. Fifteen mice were randomized into three groups: intact, denervated-insulin-like growth factor-1-treated (D-IGF-1) and denervated-nerve growth factor-treated (D-NGF). In denervated animals, the left sides were used as a control by injecting balanced salt solution (HBSS), while the right sides were injected with growth factors. The mean wet weight and the mean wet weight/body weight were significantly higher in D-IGF-1 muscles compared to the D-NGF and D-HBSS muscles, but were not different from the muscle of intact controls. Physiologic testing showed that the mean maximal tetanic twitch strength and the mean maximal fast twitch strength were also significantly higher in the D-IGF-1 muscles than in the D-NGF and D-HBSS muscles. Mean time-to-peak was significantly only decreased in the D-NGF muscles. Histological studies found that the mean percentage of type 2 fiber was significantly higher in D-NGF muscles. The types I and II mean diameters in the D-IGF-1 muscles were larger than in the D-NGF and D-HBSS muscles, but all denervated muscles had higher interstitial fibrosis than the intact controls. In conclusion, we show that IGF-1 can effectively retard denervated muscle atrophy by increasing types I and II fibre muscle diameter. However, IGF-1 cannot prevent interstitial fibrosis in the denervated muscle.

Commercial mouse and human nerve growth factors contain nerve growth factor prohormone isoforms

1997 ◽  
Vol 76 (1) ◽  
pp. 75-81 ◽  
Author(s):  
M. Reinshagen ◽  
I. Geerling ◽  
J. Lakshmanan ◽  
H. Rohm ◽  
M.P. Lutz ◽  
...  
Keyword(s):  
Growth Factors ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth ◽  
Nerve Growth Factors ◽  
Human Nerve

scholarly journals Altered Brain Expression of Insulin and Insulin-Like Growth Factors in Frontotemporal Lobar Degeneration: Another Degenerative Disease Linked to Dysregulation of Insulin Metabolic Pathways

ASN NEURO ◽  
2019 ◽  
Vol 11 ◽  
pp. 175909141983951 ◽  
Author(s):  
Connie J. Liou ◽  
Ming Tong ◽  
Jean P. Vonsattel ◽  
Suzanne M. de la Monte
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Frontotemporal Lobar Degeneration ◽  
Enzyme Linked Immunosorbent Assay ◽  
Insulin Like Growth Factor ◽  
Receptor Kinase ◽  
Nerve Growth ◽  
Neurotrophin 3 ◽  
Tgf Β1 ◽  
Igf Signaling

Background Frontotemporal lobar degeneration (FTLD) is the third most common dementing neurodegenerative disease with nearly 80% having no known etiology. Objective Growing evidence that neurodegeneration can be linked to dysregulated metabolism prompted us to measure a panel of trophic factors, receptors, and molecules that modulate brain metabolic function in FTLD. Methods Postmortem frontal (Brodmann’s area [BA]8/9 and BA24) and temporal (BA38) lobe homogenates were used to measure immunoreactivity to Tau, phosphorylated tau (pTau), ubiquitin, 4-hydroxynonenal (HNE), transforming growth factor-beta 1 (TGF-β1) and its receptor (TGF-β1R), brain-derived neurotrophic factor (BDNF), nerve growth factor, neurotrophin-3, neurotrophin-4, tropomyosin receptor kinase, and insulin and insulin-like growth factor-1 (IGF-1) and insulin-like growth factor-2 (IGF-2) and their receptors by direct-binding enzyme-linked immunosorbent assay. Results FTLD brains had significantly elevated pTau, ubiquitin, TGF-β1, and HNE immunoreactivity relative to control. In addition, BDNF and neurotrophin-4 were respectively reduced in BA8/9 and BA38, while neurotrophin-3 and nerve growth factor were upregulated in BA38, and tropomyosin receptor kinase was elevated in BA24. Lastly, insulin and insulin receptor expressions were elevated in the frontal lobe, IGF-1 was increased in BA24, IGF-1R was upregulated in all three brain regions, and IGF-2 receptor was reduced in BA24 and BA38. Conclusions Aberrantly increased levels of pTau, ubiquitin, HNE, and TGF-β1, marking neurodegeneration, oxidative stress, and neuroinflammation, overlap with altered expression of insulin/IGF signaling ligand and receptors in frontal and temporal lobe regions targeted by FTLD. Dysregulation of insulin-IGF signaling networks could account for brain hypometabolism and several characteristic neuropathologic features that characterize FTLD but overlap with Alzheimer’s disease, Parkinson’s disease, and Dementia with Lewy Body Disease.

scholarly journals Inhibition of Ethanol Neurotoxicity by Treatment with Growth Factors and Estrogen

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Jason Zell ◽  
Jeremy Montague ◽  
Tomas Lopez ◽  
Mudd Laura
Keyword(s):  
Growth Factors ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Ethanol Ingestion ◽  
Fetal Alcohol ◽  
Simultaneous Treatment ◽  
Nerve Growth ◽  
Neuronal Viability ◽  
Igf I

Ethanol ingestion by pregnant women is the primary cause of fetal alcohol syndrome, which is characterized by brain abnormalities and decreased mental capacity. In the present study,cultured neurons from embryonic rat cortices were used to study the effects of ethanol on cell survival and the potential for neuroprotection by certain growth factors and estrogen. Neurons were grown in the presence of a glial plane and in the absence of serum. Survival was assessed following chronic treatment with ethanol (45 mM) in the presence and absence of either nerve growth factor (NGF, 100ng/ml), basic fibroblast growth factor (bFGF, 5ng/ml), insulin-like growth factor I or II (IGF-I, IGF-II, both 10ng/ml), or estrogen (Es, 10nM) added on days one and four in vitro. On day in vitro 4 (DIV4) ethanol effects on neuronal viability were significantly prevented by NGF, bFGF, IGF-I, and Es. DIV6 survival of ethanol-treated neurons was increased significantly by treatment with NGF, bFGF, IGF-I, IGF-II, and Es. Nerve growth factor, bFGF, and IGF-I effects were shown to be dose-dependent. Administration of 1-100 ng/ml NGF, 0.05-5 ng/ml bFGF and 0.1-10ng/ml IGF-I led to statistically significant effects at 10, 5, and 1 ng/ml, respectively. Thus, ethanol’s effect on neuronal survival may be inhibited by simultaneous treatment with physiological doses of these factors.

Nerve growth factor regulates gene expression by several distinct mechanisms

1989 ◽  
Vol 9 (1) ◽  
pp. 135-143
Author(s):  
K O Cho ◽  
W C Skarnes ◽  
B Minsk ◽  
S Palmieri ◽  
L Jackson-Grusby ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factors ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cholera Toxin ◽  
Phorbol Myristate Acetate ◽  
Kinase Inhibitor ◽  
Transcriptional Level ◽  
Myristate Acetate ◽  
Nerve Growth

To help elucidate the mechanisms by which nerve growth factor (NGF) regulates gene expression, we have identified and studied four genes (a-2, d-2, d-4, and d-5) that are positively regulated by NGF in PC12 cells, including one (d-2) which has previously been identified as a putative transcription factor (NGF I-A). Three of these genes, including d-2, were induced very rapidly at the transcriptional level, but the relative time courses of transcription and mRNA accumulation of each of these three genes were distinct. The fourth gene (d-4) displayed no apparent increase in transcription that corresponded to the increase in its mRNA, suggesting that NGF may regulate its expression at a posttranscriptional level. Thus, NGF positively regulates gene expression by more than one mechanism. These genes could also be distinguished on the basis of their response to cyclic AMP. The expression of d-2 and a-2 was increased by cholera toxin and further augmented by NGF; however, cholera toxin not only failed to increase the levels of d-5 and d-4 mRNA but also actually inhibited the NGF-dependent increase. The expression of each of these genes, including d-2 (NGF I-A), was also increased by fibroblast growth factor, epidermal growth factor (EGF), phorbol myristate acetate, and in some cases insulin, showing that the regulation of these genes is not unique to NGF. Because each of these genes was expressed in response to phorbol myristate acetate and EGF, their expression may be necessary but is certainly not sufficient for neurite formation. The protein kinase inhibitor K-252a prevented the NGF-associated, but not the acidic FGF-associated, induction of d-2 and d-5 gene expression, suggesting that these two growth factors may regulate gene expression via different cellular pathways. The study of the regulation of the expression of these and other NGF-inducible genes should valuable new information concerning how NGF and other growth factors cause neural differentiation.

Sign in / Sign up

Export Citation Format

Share Document