Int J Mol Sci. Myopic macular schisis has other namesmyopic traction maculopathy or myopic foveoschisis. Congenital retinoschisis mostly affects people assigned male at birth (AMAB). Nature. Astrocytes help form the physical structure of the brain, and are thought to play a number of active roles, including the secretion or absorption of neural transmitters and maintenance of the bloodbrain barrier. 2018;12:206. RNA sequencing and bioinformatics analysis revealed that TPM1 altered gene signatures in glial cells including microglia and astrocytes, and regulated genes that were associated with inflammation-related pathways in TREM2/ retinas. TPM1 and Trem2 plasmids and the corresponding control plasmids were constructed by UBIGENE (USA) and Synbio Technologies (China), respectively. [5] [12] In a review of children with iCSNB only 54% of patients presented with nyctalopia and thus it is important for clinicians to not "rule out" CSNB from the differential if there is no complaint of nyctalopia. Following TPM1 knockdown (Fig. 2018;136(4):389-398. Ongoing excitation can also induce ERK and JNK activation, resulting in release of several inflammatory factors. 2018;12:206. The B-scan will give your doctor structural information about your eye. Article 8Q). Data are presented as meanSEM and analyzed by one-way ANOVA with Tukeys multiple comparison test (compared to PBS or LPS+siCTR, *p<0.05, ***p<0.001). In this study, we demonstrated in addition to its crucial roles in the regulation of neurite outgrowth, branching and synapse formation in neurons [32], the actin-associated protein TPM1 played a previously unanticipated role in regulating pro-inflammatory genes in microglia. Google Scholar. Loss of central (foveal) vision or side (peripheral) depending on where the split occurs. Multi-focal ERG shows a depression in both A-waves and B-waves in the affected retina, lending evidence that both the outer and inner retina are Vajaranant T, Szlyk J, Pulido J. Sequential Multifocal Electroretinogram Findings in a Case of Purtscher-like Retinopathy. Indeed, we observed that TPM1 overexpression failed to downregulate phosphorylated CREB (p-CREB) in BV2 cells after treatment with dbcAMP, an activator of PKA (Fig. Google Scholar. S2AG) and in vivo (Fig. Kwon HS, Koh SH. The most prominent genes activated by FGF-1 treatment include the genes responsible for the synthesis of FABP6 and FABP7 by astrocytes. 6G, H). Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations. This effect is consistent with our results in which TREM2 knockout resulted in upregulation of inflammatory mediators in response to LPS stimulation. I, J Quantification of PKA (I) and CREB (J) protein levels in BV2 cells after transfection with siCTR, siTPM1-1 or siTPM1-2 followed by LPS and H89 treatment. Li R, Liang Y, Lin B. Accumulation of systematic TPM1 mediates inflammation and neuronal remodeling by phosphorylating PKA and regulating the FABP5/NF-B signaling pathway in the retina of aged mice. Enter your library card number to sign in. Astrocytomas are divided into two categories: low grade (I and II) and high grade (III and IV). Fibrillary astrocytomas commonly occur in younger people, who often present with seizures. Taylor X, Cisternas P, You Y, You Y, Xiang S, Marambio Y, et al. The following article will detail the disease, its etiology, risk factors, pathophysiology, signs, symptoms, physical exam findings, diagnosis, prevention, treatment, and prognosis. Therefore, manipulation in TPM1 expression by either a pharmacological intervention targeting specific TPM1 or virus-mediated suppression of TPM1 could provide a unique avenue to gently restore balance in disrupted TPM1 systems to slow down the pathogenetic progression in neurodegenerative diseases including AD. Correspondence to (2008). It happens in people who have severe myopia (nearsightedness). Star-shaped, their many processes envelop synapses made by neurons. For plasmid transfection, 2 ug plasmid was co-transfected with 8l TransIntro PL Transfection Reagent (TransGen, China) or Lipofectamine 3000 (Invitrogen) in serum-free Opti-MEM medium (Thermo Fisher, USA) for 46h, followed by changing complete culture medium. This type often has astrocytic endfoot processes that physically connect the cells to the outside of capillary walls when they are in proximity to them. 8C, D), further suggesting that TREM2 signals upstream of TPM1. 2011;2(6): e173. This idea, although true, is an oversimplification of pain transduction. Learn what it means if the results are abnormal. This view states that astrocyte dysfunction may result in improper neural circuitry, which underlies certain psychiatric disorders such as autism spectrum disorders and schizophrenia.[50][5]. Mechanistically, we found that LPS treatment significantly increased mRNA levels of Bax (65.2%) and Caspase-3 (70.66%), which are associated with cell apoptosis, in siCTR-treated TREM2/ retinas compared to PBS-treated TREM2/ control retinas (Fig. Studies carried out by Hochstim and colleagues have demonstrated that three distinct populations of astrocytes arise from the p1, p2 and p3 domains. Yeh FL, Hansen DV, Sheng M. TREM2, microglia, and neurodegenerative diseases. polarization A standard ophthalmic exam is a comprehensive series of tests that checks your vision and eye health. S4H, I). 2020;9(1):42. Surprisingly, we found that TPM1 knockdown ameliorated LPS-induced inflammation in the WT retina but markedly aggravated LPS-induced inflammation, neuronal death and function decline in the TREM2/ mouse retina. 2I, J), even though latency remained unchanged (Additional file Your provider may consider this condition to be benign, which means that the condition may not be serious enough to need treatment. 2002;134 (1):125128. Fan YY, Huo J. A1/A2 astrocytes in central nervous system injuries and diseases: angels or devils? The dendritic processes of astrocytes in the WT mouse retina are entirely restricted to the nerve fiber layer (NFL) [19]. 3AE), and enhanced microglia and astrocyte activation in LPS-treated TREM2/ mouse retinas relative to siCTR- and LPS-treated TREM2/ controls (Fig. In humans, a single astrocyte cell can interact with up to 2 million synapses at a time. As the leading cause of vision loss, macular degeneration is best treated by preventing the condition or catching it early to stop further progression. Benefits from Optimal Orgasms (the Tao of Sexual Orgasms): Orgasm triggers the pituitary to release prolactin.Although chronically excessive prolactin can disable the sexual function, induce cancerous development, screw up the reproduction system and cause depression, an optimal prolactin release from your pituitary and eyes, as a result of an orgasm, is good for hGH The longest follow up documented in the literature is a patient who was followed for 38 years. The work of international groups, tradition, and flexibility combine to provide an approach that attempts to balance official systems and actual usage. Similarly, we observed that intraperitoneal injection of LPS induced TPM1 upregulation (Additional file 3: Fig. By using this website, you agree to our Three independent experiments were performed. Una onda electromagntica es una onda transversal compuesta por un campo elctrico y un campo magntico simultneamente. [71] An aging-associated change in astrocyte function might contribute to this change in dopaminergic activity. [65] However, the exact nature of this stress is uncertain. [6] Data suggest that astrocytes also signal to neurons through Ca2+-dependent release of glutamate. J Neurosci. Pilocytic astrocytomas frequently have cystic portions filled with fluid and a nodule, which is the solid portion. BG The expression levels of DEGs associated with M1 (B) or M2 microglia (C, D) and with A1 (E) or A2 astrocytes (F, G) in WT mice after treatment with PBS, or with LPS and siTPM1-1 or siCTR. As the leading cause of vision loss, macular degeneration is best treated by preventing the condition or catching it early to stop further progression. As previously described the ERG is crucial to distinguish the four subtypes of CSNB and also assists in distinguishing between cCSNB and iCSNB. Nat Genet 1999; 22: pp. Anesthetic drops will be used to numb your eye and minimize discomfort. The latter supports the existence of a threshold. Acquired senile retinoschisis of the peripheral retina imaged by spectral domain optical coherent tomography. After 10-min light adaptation under background intensity at 30cds/m2, photopic ERG was recorded at 3 and 10cds/m2 light intensities. If results are abnormal, your doctor will need to determine the cause. In response to nerve damage, heat shock proteins (HSP) are released and can bind to their respective TLRs, leading to further activation. RL and BL analyzed data and wrote the main manuscript text. Your doctor will make sure the measurements of your eye taken from the A-scan are within the normal range. 5E), which was confirmed by WB analysis (Fig. Functional assessments are a fundamental part of the clinical evaluation of patients with inherited retinal diseases (IRDs). This test uses light waves to create images of the retina. This remarkable cure of diabetes mellitus is mediated by astrocytes. Star-shaped, their many processes envelop synapses made by neurons. [14] They are presumed to contain 11-cis retinal precursors (retinoids) and exist from the RPE/Bruch membrane complex to outer nuclear layer. Interestingly, we observed that TREM2 deficiency upregulated TPM1 (Additional file 4: Fig. 3FJ). [3] Another study reports that astrocytes are the most numerous cell type in the brain. Google Scholar. C57BL/6 mice (Stock no: 000664), TREM2/ mice (Stock no: 027197), CX3CR1CreER mice (Stock no: 021160) and Rosa26iDTR mice (Stock no: 007900) were obtained from the Jackson Laboratory, USA. TPM1 knockdown exacerbates inflammation in the TREM2/ mouse retina. 8GK), indicating that TREM2 potentially regulates TPM1-induced inflammation. During a B-scan, youll be sitting with your eyes closed. Choose this option to get remote access when outside your institution. Approximately 50% of all brain tumors are glioblastomas. The pipette was kept inside the vitreous for a few seconds after the injection to prevent reflux of siRNA solution. For quantification of microglial cells, four sampling areas with 638.9m638.9m squares along the dorsalventral axis of retinal whole-mounts at 200m and 1mm from the optic nerve head on both sides were photographed, and the numbers of Iba-1+ and of CD68+Iba-1+ microglial cells were manually counted. Functionally, we found that LPS treatment significantly decreased the amplitudes of a- and b-waves of electroretinogram (ERG) under both scotopic and photopic conditions compared to WT controls (Fig. Indeed, we found that co-transfection of TPM1 and TREM2 plasmids significantly reduced TPM1 expression relative to transfection of TPM1 alone (Additional file 8: Fig. Miscellaneous Cellular and Biochemical Terms. Retinal pigment epithelium (RPE) responses are measured with an EOG test with skin-contact electrodes placed near the canthi. The following article will detail the disease, its etiology, risk factors, pathophysiology, signs, symptoms, physical exam findings, diagnosis, prevention, treatment, and prognosis. Coronary Artery Angiographic Classifications. Here is a detailed review of 8 nutrients that can help maintain proper eye function, protect your eyes from damage and fight the negative effects of. Mattapallil MJ, Wawrousek EF, Chan CC, Zhao H, Roychoudhury J, Ferguson TA, et al. Electroretinography measures the electrical responses of various cell types in the retina, including the photoreceptors (rods and cones), inner retinal cells (bipolar and amacrine cells), and the ganglion cells. Usually, they go away within a few days as your eyes adjust to your new prescription. Presentation of TRPM1-Associated Congenital Stationary Night Blindness in Children. Alzheimers -secretase (BACE1) regulates the cAMP/PKA/CREB pathway independently of -amyloid. These factors increase the responsiveness of the dorsal horn pain-projection neurons to ensuing stimuli, termed "spinal sensitization," thus amplifying the pain impulse to the brain. Splits can occur in the center of the retina but are more likely at the periphery (outer edges). S8AD), suggesting that TPM1 might regulate inflammatory responses downstream of TREM2. To specifically investigate the role of microglia in TPM1-mediated inflammation, we genetically eliminated microglia from the retina. PubMed Central KP Western blot analysis (K) and quantification of p-PKA, PKA, p-CREB, CREB and TPM1 (LP) in C57BL/6J mice following treatments with PBS, or with LPS and siTPM1-1 or siCTR. Leptin-sensitive neurons regulate appetite and body weight. Compared to CSNB, which is nonprogressive, retinitis punctata albescence is progressive and leads to increasing symptoms and gradual deterioration of ERG and visual fields. Am J Ophthalmol 2000; 130: pp. A congenital condition is something youre born with. Collectively, we have revealed two distinct roles of CREB in mediating the induction of pro-inflammatory genes in TREM2/ retinas and anti-inflammatory genes in WT retinas. However, it remains unclear how endogenous TPM1 triggers neuroinflammation in the retina. Meanwhile, we observed that TPM1 overexpression increased expression levels of pro-inflammatory cytokines and chemokines but failed to induce the inflammation in the presence of TAK242, a specific inhibitor of TLR4, suggesting the direct involvement of TLR4 in TPM1-regulated inflammation. [5][6] Known mutations for Riggs-type CSNB include autosomal dominant mutations in GNAT1 and PDE6B which are involved in rod phototransduction. Shibboleth / Open Athens technology is used to provide single sign-on between your institutions website and Oxford Academic. Cells. PubMed It appears as a-waves and b-waves. A biosignal is any signal in living beings that can be continually measured and monitored.The term biosignal is often used to refer to bioelectrical signals, but it may refer to both electrical and non-electrical signals. Low grade tumors are more common in children, and high grade tumors are more common in adults. Data are presented as meanSEM and analyzed by one-way ANOVA with Tukeys multiple comparison test (compared to PBS, *p<0.05). Five independent experiments were performed. 2016;1863(6 Pt A):121827. Consistently, CREB is previously reported to play many different roles in immune function, and CREB mediates pro-inflammatory genes, such as IL-6 [45, 46], and anti-inflammatory genes, such as IL-10 [47, 48], as well. Article 666-15 (MedChemExpress) was dissolved in 10% DMSO and 90% corn oil, and TREM2/ mice (45weeks) were treated with a vehicle or 666-15 at 20mg/kg via intragastric gavage for five times, 2days apart. 6E, F). Taken together, these data indicate that TPM1 potentially regulates neuroinflammation via the PKA/CREB signaling pathway. Astrocytes (from Ancient Greek , stron, "star" + , ktos, "cavity", "cell"), also known collectively as astroglia, are characteristic star-shaped glial cells in the brain and spinal cord. [2], Inherited retinal degenerations in which the ERG can be useful include:[citation needed]. Receiving a macular degeneration diagnosis can be scary. 2010;22(5):87181. The multifocal ERG is used to record separate responses for different retinal locations. Western blot analysis was performed as previously described [32, 56]. Nat Med. 3AE). In addition, we observed that LPS treatment deactivated the PKA/CREB signaling pathway in BV2 cells by downregulating phosphorylation of both PKA and CREB (Additional file 2: Fig. AC Western blot analysis (A) and quantification of p-CREB and CREB (B, C) in TREM2/ mice after treatments with LPS and 666-15, a potent and selective CREB inhibitor. How to prepare for an eye and orbit ultrasound, cpmc.org/learning/documents/bscan-ws.html, mayoclinic.org/diseases-conditions/eye-melanoma/basics/tests-diagnosis/con-20027875, eyewiki.aao.org/Ophthalmologic_Ultrasound, onlinelibrary.wiley.com/doi/10.1111/j.1442-9071.2008.01892.x/full. 8C, D), which is in line with previous observations [29, 30], and TPM1 knockdown did not reverse this trend (Fig. 2020;17(1):223. The datasets used and analyzed during the current study are available from the corresponding author on reasonable request. S6B). 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[4] Fundus albipunctatus and Oguchi disease are two entities within CSNB that are associated with fundus findings. As noxious pain is sustained, spinal sensitization creates transcriptional changes in the neurons of the dorsal horn that lead to altered function for extended periods. Collectively, these results suggest that TPM1 knockdown promotes additional increase in neuroinflammation and more cell apoptosis in TREM2-deficient mouse retinas following LPS treatment. Mol Immunol. The B-scan helps your doctor see the space behind the eye. A simple example of a polarized transverse wave is vibrations traveling along a taut string (see image); for example, in a musical Taken together, our data demonstrated that TPM1 was involved in LPS-induced inflammation and functional decline via mediating the PKA/CREB signaling pathway (Fig. Two major functions of rhodopsin phosphorylation have been School of Optometry, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong, Rong Li,Jing Zhang,Meng Cheng&Bin Lin, Centre for Eye and Vision Research (CEVR), 17W Hong Kong Science Park, Shatin, Hong Kong, Research Centre for SHARP Vision (RCSV), The Hong Kong Polytechnic University, Kowloon, Hong Kong, You can also search for this author in Collectively, our results demonstrate that TPM1 is an important regulator of pro-inflammatory gene expression in microglia and that TPM1 could be a potential target for therapeutic intervention in brain diseases. Zhao Y, Yi W, Lu Y, Li W, Wang H. Lipopolysaccharide induces BV2 microglial cell migration via a decrease in SET8 expression. Once the specific subtype of CSNB has been elucidated based on clinical and ERG findings, selective gene testing can be procured. These results confirm that CREB promotes pro-inflammatory responses in the TREM2/ retina through overexpression of pro-inflammatory cytokines, such as IL-6, which has been associated with inflammatory and neurodegenerative processes [27, 28]. Astrocyte pathology in the hippocampus thus might make a contribution to the pathology of Alzheimer's disease. However, we observed that TPM1 knockdown failed to suppress the inflammation elicited by microglia depletion, suggesting that the inflammation elicited by microglia depletion is mediated probably by other type of glial cells via other signaling pathways, such as astrocytes, and that TPM1 potentially regulates inflammation majorly through microglia. Functionally, we observed decreases in the amplitudes of a- and b-waves of ERG in LPS-treated TREM2/ mice under both scotopic and photopic conditions (Fig. Learn more about the exam and its uses. ), (https://www.asrs.org/patients/retinal-diseases/14/congenital-x-linked-retinoschisis), (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6786223/#:~:text=Bullous%20or%20reticular%20retinoschisis%20is,accompanied%20with%20rhegmatogenous%20retinal%20detachment.). The protoplasmic glia are the most prevalent and are found in grey matter tissue, possess a larger quantity of organelles, and exhibit short and highly branched tertiary processes. An ultrasound technician or an ophthalmologist (a doctor who specializes in diagnosing and treating eye disorders and diseases) usually performs the procedure (sometimes called eye studies). Microglia, the principal resident immune cells of the central nervous system (CNS), serve as sensors and executers of innate immunity. Your eye doctor will advise you not to rub your eyes until the anesthetic has completely worn off. [12] James Dewar and John Gray McKendrick independently suggested that the biological potential was from retina. Ringeisen AL. No pain is associated with the procedure. 2AH) results. When on the institution site, please use the credentials provided by your institution. We further showed that TPM1 exerted its effect via the PKA/CREB pathway in the WT retina. FH, Retina whole-mounts stained with antibodies against Iba-1 and CD68 (F) and quantification of numbers of Iba-1+ (G) and of Iba-1+CD68+ microglia (H) in the IPL and OPL of TREM2/ retinas after treatments with PBS, or with LPS and siTPM1-1 or siCTR. [66] Thus, a connection between these two glial features is apparent. B, C Western blot analysis (B) and quantification of CD68 (C) in BV2 cells after TPM1 transfection. Ahmed Z, Kalinski H, Berry M, Almasieh M, Ashush H, Slager N, et al. The difference is due to residual rod function. polarization This test uses light waves to create images of the retina. Star-shaped, their many processes envelop synapses made by neurons. A, B DEGs related to the CREB signaling in neurons in WT (A) or TREM2/ mice (B) following treatments with PBS, or with LPS and siTPM1-1 or siCTR. An increase in intracellular calcium concentration can propagate outwards through this functional syncytium. 2010;47(78):1396403. Neuroinflammation and microglia: considerations and approaches for neurotoxicity assessment. 4DS), suggesting that TPM1 knockdown further enhances glial cell reactivity in LPS-treated TREM2/ retinas, which is consistent with morphological alterations in microglia and astrocytes (Fig. The dim flash scotopic ERG is flat whereas the strong flash scotopic ERG shows a decreased a-wave and b-wave amplitude which is in contradistinction to the Schubert-Bornstein which demonstrates a normal a-wave. The study concludes that, if verified by further research, "ERG could provide the neurotransmitter specificity of PET at a much lower cost". was kindly supported by General Research Fund (GRF) from the Hong Kong Research Grants Council, the Health and Medical Research Fund (HMRF) of Hong Kong Food and Health Bureau, and Project of Strategic Importance of The Hong Kong Polytechnic University. Remarkably, we found that TPM1 knockdown further elevated GFAP immunoreactivity and astrocyte activation in LPS-treated TREM2/ mice compared to LPS-treated TREM2/ control mice (Fig. Nat Genet 1997; 15: pp. Importantly, the ERG is an objective measure of retinal function that can be recorded non-invasively under physiological conditions. 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This helps determine the correct lens implant for cataract surgery. We found that TPM1 knockdown increased the numbers of activated microglia (Iba-1+CD68+) in the OPL of LPS-treated TREM2/ mouse retinas relative to siCTR- and LPS-treated group (Fig. Consistently, previous studies reported TPM1 expression in neurons of the brain [49, 50]. 6D), suggesting that TLR4 could be involved in TPM1-mediated inflammation in TREM2/ mice. Li R, Sahu S, Schachner M. Phenelzine, a small organic compound mimicking the functions of cell adhesion molecule L1, promotes functional recovery after mouse spinal cord injury. PubMed Suppression of retinal neovascularization by erythropoietin siRNA in a mouse model of proliferative retinopathy. Arrowheads show the colocalization of Iba-1-positive microglial cells with CD68 signal. 646-656, Genead MA, Fishman GA, and Lindeman M: Spectral-domain optical coherence tomography and fundus autofluorescence characteristics in patients with fundus albipunctatus and retinitis punctata albescens. It will also provide newest advancements and 2019;10(3):66475. 6D), and those genes were further elevated in LPS-treated TREM2/ mice following siTPM1 treatment, indicating that TPM1 knockdown leads to the enhancement of LPS-induced neuroinflammation in TREM2/ mice, which is consistent with our in vivo results (Fig. Functional assessments are a fundamental part of the clinical evaluation of patients with inherited retinal diseases (IRDs). J Neuroinflamm. Alluin O, Delivet-Mongrain H, Gauthier MK, Fehlings MG, Rossignol S, Karimi-Abdolrezaee S. Examination of the combined effects of chondroitinase ABC, growth factors and locomotor training following compressive spinal cord injury on neuroanatomical plasticity and kinematics. Bulk RNA sequencing was performed with DNBSEQ (DNBSEQ Technology) platform. The range of services is very broad and can include education, fellowship and technological help. 2009;50(3):132935. An altered glial function in this region could compromise the function of dentate gyrus neurons and also the function of axons that terminate in the dentate gyrus. TLR4 induces CREB-mediated IL-6 production via upregulation of F-spondin to promote vascular smooth muscle cell migration. Data are presented as meanSEM, unpaired two-tailed Students t test (control plasmid vs. Trem2 plasmid, *p<0.05). An intense sharp negative wave appear in epileptic seizures and during reflexes. Triggering receptor expressed on myeloid cells 2 (TREM2) is specifically expressed by microglia in the brain [8]. Schevzov G, Whittaker SP, Fath T, Lin JJ, Gunning PW. Furthermore, we identified that TPM1 regulated inflammation downstream of TREM2 and in a microglia-dependent manner. Eye studies can be done in an office, outpatient imaging center, or hospital. For example, GP astrocytes are in close contact with neurons that make a neurotransmitter called dopamine in both the rat and human hypothalamus. Additional Readings and General References. Furthermore, we observed that LPS administration significantly elevated the expression of p-CREB but not p-PKA and PKA in TREM2/ retinas (Fig. We found that LPS significantly stimulated endogenous TPM1 expression (Additional file 2: Fig. However, TPM1 knockdown partially rescued LPS-induced function declines on WT mice (Fig. Triggering receptor expressed on myeloid cells 2. Peng B, Xiao J, Wang K, So KF, Tipoe GL, Lin B. Suppression of microglial activation is neuroprotective in a mouse model of human retinitis pigmentosa. The A-scan ultrasound takes measurements of your eye. After TPM1 knockdown, p-CREB also showed an increase trend in LPS-treated TREM2/ retinas relative to siCTR- and LPS-treated TREM2/ control retinas (Fig. We first performed the scotopic ERG on dark-adapted mice with different light intensities at 0.01, 0.1, 1 and 3cds/m2. In their results they were able to see that astrocytes had a direct role in Long-term potentiation with the mixed culture (which is the culture that was grown from a layer of astrocytes) but not in GCM cultures. Two major functions of rhodopsin phosphorylation have been Last medically reviewed on November 22, 2017. S1G, H; Additional file 2: Fig. Garrison and co-workers[51] were the first to suggest association when they found a correlation between astrocyte hypertrophy in the dorsal horn of the spinal cord and hypersensitivity to pain after peripheral nerve injury, typically considered an indicator of glial activation after injury. TPM1 mediates inflammatory responses downstream of TREM2. NQ Western blot analysis (N) and quantification of p-PKA, p-CREB, and TPM1 (OQ) in BV2 cells after transfection with siTPM1-1, siTPM1-2, or siCTR followed by LPS and H89 treatment. 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