Serping1 associated with α-synuclein increase in colonic smooth muscles of MPTP-induced Parkinson's disease mice.

Patients with Parkinson's disease (PD) have gastrointestinal motility disorders, which are common non-motor symptoms. However, the reasons for these motility disorders remain unclear. Increased alpha-synuclein (α-syn) is considered an important factor in peristalsis dysfunction in colonic smooth muscles in patients with PD.

Association between Decreased SGK1 and Increased Intestinal α-Synuclein in an MPTP Mouse Model of Parkinson's Disease.

Parkinson's disease (PD) is a globally common progressive neurodegenerative disease resulting from the loss of dopaminergic neurons in the brain. Increased α-synuclein (α-syn) is associated with the degeneration of dopaminergic neurons and non-motor symptoms like gastrointestinal disorders. In this study, we investigated the association between serum/glucocorticoid-related kinase 1 (SGK1) and α-syn in the colon of a PD mouse model.

Association between SGK1 and α-synuclein in skeletal muscle in an MPTP-induced Parkinson's disease model.

Parkinson's disease (PD) is a neurodegenerative disease caused by loss of dopaminergic neurons in the substantia nigra and it is known to involve the accumulation of α-synuclein (α-syn), which is a neuroprotein that promotes degeneration of dopaminergic neurons. Serum/glucocorticoid-related kinase 1 (SGK1) is involved in the physiological and pathological processes in neurons. The aim of this study was to examine the relationship between SGK1 and α-syn expression in muscle tissue of a PD model and in C2C12 cells.

The Effects of Serping1 siRNA in α-Synuclein Regulation in MPTP-Induced Parkinson's Disease.

Our understanding of the gastrointestinal system in the pathophysiology of Parkinson's disease (PD) has grown considerably over the last two decades. Patients with PD experience notable gastrointestinal symptoms, including constipation. In this study, the effects of knocked-down serping1, associated with the contraction and relaxation of smooth muscle and inflammation responses, by applying the serping1 siRNA were investigated in 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine-induced PD mice in an α-syn change aspect.

Association Between Decreased Srpk3 Expression and Increased Substantia Nigra Alpha-Synuclein Level in an MPTP-Induced Parkinson's Disease Mouse Model.

Parkinson's disease (PD) is the second most common neurodegenerative disorder and is caused by the loss of dopaminergic neurons in the substantia nigra (SN). However, the reason for the death of dopaminergic neurons remains unclear. An increase in α-synuclein (α-syn) expression is an important factor in the pathogenesis of PD.

Decrease in Levels Is Associated with an Increase in α-Synuclein Levels in an MPTP-Induced Parkinson's Disease Mouse Model and SH-SY5Y Cells.

We investigated the potential association between  ITGA7) and alpha-synuclein (α-syn) in a methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease (PD) mouse model. Tyrosine hydroxylase (TH), ITGA7, and α-syn expression in the substantia nigra (SN) of the brain were observed to examine the pathological characteristics of PD. To determine the relationship between ITGA7 and PD, the expression of TH and α-syn was investigated after ITGA7 siRNA knockdown in SH-SY5Y cells.

Association of decreased triadin expression level with apoptosis of dopaminergic cells in Parkinson's disease mouse model.

Background: Parkinson's disease (PD) represent a loss of dopaminergic neurons in the substantia nigra (SN) of the midbrain. However, its cause remains unknown and Triadin (TRDN) function in the brain is also unknown. To examine the relationship between TRDN and PD, the expression levels of protein related to PD in TRDN knockdown status were studied in the SH-SY5Y cells.

Decrease Associated with Alpha-Synuclein Increase in Muscles of MPTP-Induced Parkinson's Disease Mice.

Parkinson's disease (PD) is characterized by a loss of dopaminergic cells in the substantia nigra, and its histopathological features include the presence of fibrillar aggregates of α-synuclein (α-syn), which are called Lewy bodies and Lewy neurites. Lewy pathology has been identified not only in the brain but also in various tissues, including muscles. This study aimed to investigate the link between serine/arginine-rich protein specific kinase 3 () and α-syn in muscles in PD.

Triadin Decrease Impairs the Expression of E-C Coupling Related Proteins in Muscles of MPTP-Induced Parkinson's Disease Mice.

Parkinson's disease (PD), caused by destruction of dopaminergic neurons in the brain, leads to motor symptoms like bradykinesia, tremor, and walking impairments. While most research effort focuses on changes in neuronal pathology we examined how muscle proteins were altered in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. A Ca release channel complex, consisting of ryanodine receptors (RYR), triadin (TRDN), and calsequestrin (CSQ1), is important for excitation-contraction coupling in the sarcoplasmic reticulum membrane in muscles.

Association of increase in Serping1 level with dopaminergic cell reduction in an MPTP-induced Parkinson's disease mouse model.

Parkinson's disease (PD) is a progressive neurodegenerative disease, which shows distinct manifestations such as significant loss of dopaminergic neurons in the substantia nigra (SN). Gene expression was analyzed in the SN of mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), wherein downregulation of dopaminergic neurons occurred to examine the possible causes leading to the loss of dopaminergic neurons. In addition, a serine/cysteine protease inhibitor (Serping1) was studied as one of the genes that were prominently upregulated in mice chronically intoxicated with MPTP.