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Proteomics and functional study reveal kallikrein-6 enhances communicating hydrocephalus
Lei Yuan1, Dongdong Zou1, Xia Yang1
1Department of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Insights
Kallikrein 6 (KLK6) is upregulated in communicating hydrocephalus (CH). Reducing KLK6 expression improves synapse structure and may offer a new therapeutic target for CH.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Communicating hydrocephalus (CH) is a prevalent neurological disorder resulting from cerebrospinal fluid pathway blockages.
- Understanding the molecular underpinnings of CH is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the molecular mechanisms involved in the development of communicating hydrocephalus (CH).
- To identify potential molecular targets for CH treatment.
Main Methods:
- Quantitative proteomic analysis to identify differentially expressed proteins (DEPs) in CH patients.
- Construction and validation of a CH rat model.
- Loss-of-function experiments using small-interfering RNA (siRNA) to assess the role of kallikrein 6 (KLK6).
- Immunofluorescence and transcriptome profiling to analyze molecular changes.
Main Results:
- Kallikrein 6 (KLK6) was significantly upregulated in CH patients and co-localized with neuronal nuclei in a CH rat model.
- Knockdown of KLK6 using siRNA improved synapse structure and increased the expression of synaptic proteins (synapsin-1, PSD95).
- Transcriptome analysis revealed upregulated differentially expressed genes (DEGs) potentially involved in synaptic recovery after KLK6 interference.
Conclusions:
- KLK6 plays a role in the pathogenesis of communicating hydrocephalus.
- KLK6 represents a potential therapeutic target for managing CH.
Background:
Communicating hydrocephalus (CH) is a common neurological disorder caused by a blockage of cerebrospinal fluid. In this study, we aimed to explore the potential molecular mechanism underlying CH development.
Methods:
Quantitative proteomic analysis was performed to screen the differentially expressed proteins (DEPs) between patients with and without CH. A CH rat model was verified by Hoechst staining, and the co-localization of the target protein and neuron was detected using immunofluorescence staining. Loss-of-function experiments were performed to examine the effect of KLK6 on the synapse structure.
Results:
A total of 11 DEPs were identified, and kallikrein 6 (KLK6) expression was found to be significantly upregulated in patients with CH compared with that in patients without CH. The CH rat model was successfully constructed, and KLK6 was found to be co-localized with neuronal nuclei in brain tissue. The expression level of IL-1β, TNF-α, and KLK6 in the CH group was higher than that in the control group. After knockdown of KLK6 expression using small-interfering RNA (siRNA), the expression levels of synapsin-1 and PSD95 in neuronal cells were increased, and the length, number, and structure of synapses were significantly improved. Following siRNA interference KLK6 expression, 5681 differentially expressed genes (DEGs) were identified in transcriptome profile. The upregulated DEGs of Appl2, Nav2, and Nrn1 may be involved in the recovery of synaptic structures after the interference of KLK6 expression.
Conclusions:
Collectively, KLK6 participates in the development of CH and might provide a new target for CH treatment.
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