Transforming growth factor-β1 levels are elevated in the striatum and in ventricular cerebrospinal fluid in Parkinson's disease

1995 ◽  
Vol 193 (2) ◽  
pp. 129-132 ◽  
Author(s):  
Makio Mogi ◽  
Minoru Harada ◽  
Tomoyoshi Kondo ◽  
Hirotaro Narabayashi ◽  
Peter Riederer ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1

scholarly journals Improvement of Impaired Motor Functions by Human Dental Exfoliated Deciduous Teeth Stem Cell-Derived Factors in a Rat Model of Parkinson’s Disease

2020 ◽  
Vol 21 (11) ◽  
pp. 3807 ◽  
Author(s):  
Yong-Ren Chen ◽  
Pei-Lun Lai ◽  
Yueh Chien ◽  
Po-Hui Lee ◽  
Ying-Hsiu Lai ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Stem Cells ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Rat Model ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Deciduous Teeth ◽  
Comprehensive Treatment

Parkinson’s disease (PD) is a long-term degenerative disease of the central nervous system (CNS) that primarily affects the motor system. So far there is no effective treatment for PD, only some drugs, surgery, and comprehensive treatment can alleviate the symptoms of PD. Stem cells derived from human exfoliated deciduous teeth (SHED), mesenchymal stem cells derived from dental pulp, may have promising potential in regenerative medicine. In this study, we examine the therapeutic effect of SHED-derived conditioned medium (SHED-CM) in a rotenone-induced PD rat model. Intravenous administration of SHED-CM generated by standardized procedures significantly improved the PD symptoms accompanied with increased tyrosine hydroxylase amounts in the striatum, and decreased α-synuclein levels in both the nigra and striatum, from rotenone-treated rats. In addition, this SHED-CM treatment decreased both Iba-1 and CD4 levels in these brain areas. Gene ontology analysis indicated that the biological process of genes affected by SHED-CM was primarily implicated in neurodevelopment and nerve regeneration. The major constituents of SHED-CM included insulin-like growth factor binding protein-6 (IGFBP-6), tissue inhibitor of metalloproteinase (TIMP)-2, TIMP-1, and transforming growth factor β1 (TGF-β1). RNA-sequencing (RNA-seq) and Ingenuity Pathway Analysis (IPA) revealed that these factors may ameliorate PD symptoms through modulating the cholinergic synapses, calcium signaling pathways, serotoninergic synapses, and axon guidance. In conclusion, our data indicate that SHED-CM contains active constituents that may have promising efficacy to alleviate PD.

scholarly journals The Immunomodulary Effects of Systematic Exercise in Older Adults and People with Parkinson’s Disease

2020 ◽  
Vol 9 (1) ◽  
pp. 184 ◽  
Author(s):  
Jadwiga Szymura ◽  
Jadwiga Kubica ◽  
Magdalena Wiecek ◽  
Joanna Pera
Keyword(s):  
Older Adults ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Balance Training ◽  
Transforming Growth Factor Β1 ◽  
Moderate Intensity ◽  
Control Groups ◽  
Necrosis Factor Alpha

We sought to investigate whether regular balance training of moderate intensity (BT) has an effect on changes in selected cytokines, neurotrophic factors, CD200 and fractalkine in healthy older adults and participants with Parkinson’s disease (PD). Sixty-two subjects were divided into groups depending on experimental intervention: (1) group of people with PD participating in BT (PDBT), (2) group of healthy older people participating in BT (HBT), (3,4) control groups including healthy individuals (HNT) and people with PD (PDNT). Blood samples were collected twice: before and after 12 weeks of balance exercise (PDBT, HBT), or 12 weeks apart (PDNT, HNT). The study revealed significant increase of interleukin10 (PDBT, p = 0.026; HBT, p = 0.011), β-nerve growth factor (HBT, p = 0.002; PDBT, p = 0.016), transforming growth factor-β1 (PDBT, p = 0.018; HBT, p < 0.004), brain-derived neurotrophic factor (PDBT, p = 0.011; HBT, p < 0.001) and fractalkine (PDBT, p = 0.045; HBT, p < 0.003) concentration only in training groups. In PDBT, we have found a significant decrease of tumor necrosis factor alpha. No training effect on concentration of interleukin6, insulin-like growth factor 1 and CD200 was observed in both training and control groups. Regular training can modulate level of inflammatory markers and induce neuroprotective mechanism to reduce the inflammatory response.

scholarly journals Transforming Growth Factor-β1 in the Cerebrospinal Fluid of Patients with Subarachnoid Hemorrhage: Titers Derived from Exogenous and Endogenous Sources

2001 ◽  
Vol 21 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Caroline Flood ◽  
James Akinwunmi ◽  
Catherine Lagord ◽  
Matija Daniel ◽  
Martin Berry ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Communicating Hydrocephalus ◽  
Specific Response ◽  
Immunosorbant Assay ◽  
Sequential Samples ◽  
Enzyme Linked Immunosorbant Assay ◽  
Tgf Β1

Transforming growth factor-β1 (TGF-β1) is a fibrogenic cytokine that is involved in postinjury repair and is implicated in the etiology of postsubarachnoid hemorrhage (SAH) chronic communicating hydrocephalus. TGF-β1 was measured by enzyme-linked immunosorbant assay (ELISA) in sequential samples of cerebrospinal fluid (CSF) in 11 patients with hydrocephalus after SAH; levels were seen to be biphasically elevated and sources were investigated. TGF-β1 levels were compared with albumin levels that estimated CSF blood content. Control samples from nonhemorrhagic hydrocephalics were tested similarly. Mean total TGF-β1 levels were elevated to 4400 ± 3435 (±SD) pg/mL greater than control levels of 97 ± 42 at 1 to 2 days posthemorrhage. Thereafter, levels fell to 714 ± 401 by 5 to 6 days posthemorrhage, then rose to a second peak of 1667 ± 774 at 9 to 10 days posthemorrhage, remaining significantly increased until 19 days posthemorrhage ( P = 0.007). The first peak probably derived from extravasated platelets and correlated with increased albumin levels in the CSF. The second TGF-β1 peak rose greater than CSF albumin levels that had stabilized at this time, and thus was attributed to a tissue-specific response rather than a re-bleed. TGF-β1 was detected in the choroid secretory epithelium from controls, but levels were greater in SAH patients at 10 to 12 days posthemorrhage. The authors conclude that the elevated levels of TGF-β1 in CSF after SAH are derived initially from blood and later from endogenous sources such as the choroid plexus.

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