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Cited by 40Neuroinflammation and Neurodegeneration MechanismsMicroRNA in disease regulationNeurological Disease Mechanisms and Treatments

miR-142-3p Regulates BDNF Expression in Activated Rodent Microglia Through Its Target CAMK2A

Open access
Gupta, Neelima, Jadhav, Shweta, Tan, Kai-Leng, Saw, Genevieve, Mallilankaraman, Karthik Babu, Dheen, S. Thameem·2020·Frontiers in Cellular Neuroscience
DOI 10.3389/fncel.2020.00132PMC PMC7253665
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Abstract

Microglia, the innate immune effector cells of mammalian central nervous system (CNS), are involved in development, homeostasis and pathology of CNS. Microglia become activated in response to various insults and injuries and protect the CNS by phagocytosing the invading pathogens, dead neurons and other cellular debris. Recent studies have demonstrated that the epigenetic mechanisms ensure the coordinated regulation of genes involved in microglial activation. In this study, we performed a microRNA (miRNA) microarray in activated primary microglia derived from rat pups brain and identified differentially expressed miRNAs targeting key genes involved in cell survival, apoptosis and inflammatory responses. Interestingly, miR-142-3p, one of the highly up-regulated miRNAs in microglia upon lipopolysaccharide (LPS)-mediated activation, compared to untreated primary microglia cells was predicted to target Ca2+/calmodulin dependent kinase 2a (CAMK2A). Further, luciferase assay confirmed that miR-142-3p targets the 3’UTR of Camk2a. CAMK2A has been implicated in regulating expression of brain-derived neurotrophic factor (BDNF) and long-term potentiation (LTP), a cellular mechanism underlying memory and learning. In view of this, this study further focused on understanding the miR-142-3p mediated regulation of CAMK2A-BDNF pathway via Cyclic AMP-responsive element-binding protein (CREB) in activated microglia. The results revealed that CAMK2A was downregulated in activated microglia suggesting an inverse relationship between miR-142-3p and Camk2a in activated microglia. Overexpression of miR-142-3p in microglia was found to decrease the expression of CAMK2A and subsequently BDNF through regulation of CREB phosphorylation. Functional analysis through shRNA-mediated stable knockdown of CAMK2A in microglia confirmed that the regulation of BDNF by miR-142-3p is via CAMK2A. Overall, this study provides a database of differentially expressed miRNAs in activated primary microglia and reveals that microglial miR-142-3p regulates CAMK2A-CREB-BDNF pathway which is involved in synaptic plasticity.

AI snapshot

Written from the paper’s full text.

TL;DR

This study profiles miRNAs in LPS-activated rat primary microglia and identifies miR-142-3p as highly upregulated. It shows that miR-142-3p targets the *Camk2a* 3′UTR and downregulates the CAMK2A-CREB-BDNF pathway in activated microglia.

Key findings

  • MicroRNA microarray in LPS-activated rat primary microglia identified top differentially expressed miRNAs, including rno-miR-142-3p (logFC 2.43, fold change 5.37, p = 6.76E-04) and rno-miR-142-5p (logFC 1.80, fold change 3.49, p = 4.08E-04) (Table 1).
  • miR-142-3p targets *Camk2a*: luciferase activity was significantly decreased in BV2 cells co-transfected with miR-142-3p mimics and a *Camk2a* 3′UTR vector; miR-142-3p overexpression decreased CAMK2A protein, while miR-142-3p inhibition increased it. Overexpression of miR-142-5p did not significantly alter CAMK2A.
  • The CAMK2A-CREB-BDNF pathway was downregulated in LPS-activated microglia: CAMK2A, pCREB, and BDNF protein levels significantly decreased, while total CREB and β-actin showed no difference.
  • miR-142-3p overexpression caused a ~50% decrease in BDNF protein, and miR-142-3p inhibition increased BDNF. shRNA-mediated CAMK2A knockdown produced a ~50% decrease in *Camk2a* mRNA and protein and downregulated pCREB and BDNF, supporting regulation of BDNF by miR-142-3p via CAMK2A.

Methods

  • Primary microglia were isolated from 3–5-day postnatal Wistar rat cerebrum and activated with LPS (1 μg/ml, 6 h); murine BV2 microglial cells were also LPS-activated. miRNA profiling used the Exiqon miRCURY LNA array with 3,100 capture probes, validated by qRT-PCR; pathway analysis used IPA and target prediction used TargetScan/Miranda.
  • Functional studies in BV2 cells used miR-142-3p/5p mimics and inhibitors, a luciferase reporter containing the mouse *Camk2a* 3′UTR, Western blotting, immunofluorescence, and lentiviral shRNA-mediated stable CAMK2A knockdown.
  • Data are presented as mean ± SD from at least three independent experiments; significance was assessed by Student’s t-test or one-way ANOVA with post hoc Tukey test at p < 0.05.

Limitations

  • The paper does not include a limitations section.
  • Evident from the text: the work is entirely in vitro, using primary rat microglia and murine BV2 cells, with no in vivo assessment of synaptic plasticity, LTP, learning, or memory.
  • Evident from the text: miRNA profiling was performed in rat primary microglia, while key functional validation and the luciferase reporter used BV2 cells and mouse *Camk2a* 3′UTR, so species and cell-model differences are not addressed.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.3389/fncel.2020.00132

Cites

75 of 75 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

1 of 24 cited sources checked · 0 supported · 0 flagged · accuracy not yet measured

  • Findingown data

    Inhibition of miR-142-3p significantly increases BDNF expression.

    “inhibition of miR-142-3p resulted in a significant increase in the expression of BDNF”
    Quote in the paperSubstantial claim
  • Findingown data

    Pathway analysis identified altered expression of several miRNAs targeting genes involved in neuroinflammation and synaptic plasticity in activated microglia.

    “the pathway analysis identified altered expression of several miRNAs targeting genes involved in neuroinflammation as well as synaptic plasticity in activated microglia”
    Quote in the paperNot a substantial claim
  • Findingown data

    CAMK2A protein expression is decreased in LPS-activated primary rat microglia at 6 h compared to control.

    “CAMK2A protein was found to be significantly decreased in primary microglia activated by LPS treatment for 6 h (Figures 4A,B).”
    • Also stated in: § CAMK2A-CREB-BDNF Pathway Is Downregulated in Activated Microglia · plain
      “These results were further verified using immunofluorescence, wherein, a stark decrease in CAMK2A expression was noticed in activated microglia when compared to control (Figure 4C).”
    • Also stated in: § CAMK2A-CREB-BDNF Pathway Is Downregulated in Activated Microglia · plain
      “Immunoblots of CAMK2A (50 kDa), phosphorylation of CREB (pCREB; 43 kDa), BDNF (15 kDa) in LPS activated primary microglia show significant downregulation.”
    Quote in the paperSubstantial claim
  • Findingown data

    In LPS-activated primary rat microglia, global miRNA profiling identified differentially expressed miRNAs compared to untreated control.

    “In this study, we performed a microRNA (miRNA) microarray in activated primary microglia derived from rat pup’s brain and identified differentially expressed miRNAs targeting key genes involved in cell survival, apoptosis, and inflammatory responses.”
    • Also stated in: § Global miRNA Expression Profile Shows Differential Expression of miRNAs in Activated Microglia · plain
      “We have identified and clustered the top 50 differentially expressed miRNAs in activated rat primary microglia compared to control, after stringent selection criteria applied (Figure 1A, Table 1).”
    • Also stated in: § Introduction · boosted
      “In the current study, we demonstrate that activation of microglia by lipopolysaccharide (LPS) is associated with the altered miRNA expression profile.”
    Quote in the paperSubstantial claim
  • Findingown data

    Knockdown of CAMK2A leads to consistent downregulation of CAMK2A, pCREB, and BDNF at protein level compared to negative control.

    “A consistent downregulation of CAMK2A, pCREB, and BDNF at the protein level was observed in microglia after knockdown of CAMK2A compared to a negative control.”
    Quote in the paperSubstantial claim
  • Classified as probably not a substantial claim. 19
  • May combine two claims. 10
  • The quote only partly states this claim. 1

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    miRNAs targeting several genes regulate microglia behavior and functions in diverse CNS pathologies.

    “Recently, miRNAs targeting several genes are involved in regulating microglia behavior and functions in diverse CNS pathologies including ischemic brain injuries (Selvamani et al., 2012; Zhao et al., 2013; Karthikeyan et al., 2018), multiple sclerosis (Ponomarev et al., 2011) and prion disease (Saba et al., 2012; Slota and Booth, 2019).”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites Selvamani et al., 2012 source

      The Results (no page available) show that anti-Let7f increased IGF-1 production in microglia harvested from ischemic cortex. The Discussion proposes that this may alter microglial activation, but does not establish broad regulation of microglial behavior and functions by miRNAs targeting several genes. This source supports an ischemic-injury example, not the broader claim by itself. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites Zhao et al., 2013 source
    • cites Karthikeyan et al., 2018 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    miR-101 and miR-142-3p were among the top hits in the miRNA microarray in the present study.

    “Several other miRNAs such as miR-101, miR-142-3p, which were among the top hits obtained in the miRNA microarray in the present study”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Findingown data

    miR-29b-3p, miR-21-5p, miR-19b-3p, miR-101-3p, and miR-30c-5p are upregulated in activated microglia.

    “Pathway analysis further revealed that several miRNAs including miR-29b-3p, miR-21-5p, miR-19b-3p, miR-101-3p, and miR-30c-5p, were found to be upregulated in activated microglia.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    miR-146a-5p, miR-95p, miR-223-3p, and miR-21-5p are upregulated in activated microglia.

    “Specifically, this analysis showed upregulation of miR-146a-5p, miR-95p, miR-223-3p, and miR-21-5p in activated microglia.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    NF-κB signaling pathway is upregulated in activated microglia.

    “The pathway analysis further revealed that the NF-κB signaling pathway which plays an important role in neuroinflammation was upregulated in activated microglia”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Neuroinflammation in the brain can negatively impact memory and cognitive functions through altered expression of memory-associated genes.

    “It has recently been established that neuroinflammation in the brain could negatively impact memory and cognitive functions, as a result of altered expression of memory-associated genes (Baghel et al., 2018).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Baghel et al., 2018 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    This study was approved by the National University of Singapore Institutional Animal Care and Use Committee (IACUC protocol no. R14-1643).

    “This study was approved by the National University of Singapore Institutional Animal Care and Use Committee (IACUC protocol no. R14-1643).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The quality of total RNA was verified by an Agilent 2100 Bioanalyzer profile.

    “The quality of the total RNA was verified by an Agilent 2100 Bioanalyzer profile.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    Microglia-derived BDNF contributes to maintenance of synaptic plasticity.

    “microglia derived factors such as BDNF, have been shown to contribute to the maintenance of synaptic plasticity (Harada et al., 2002; Parkhurst et al., 2013).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites Harada et al., 2002 source
    • cites Parkhurst et al., 2013 source

      Queued — the background check reaches it, usually within a day.

  • Classified as probably not a substantial claim.

    Premisecitation

    BDNF transcription is dependent on Ca2+ mediated activation of CREB.

    “BDNF transcription is dependent on Ca2+ mediated activation of cAMP-response element-binding protein (CREB; Tao et al., 1998).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Tao et al., 1998 source

  • Classified as probably not a substantial claim.

    Premisecitation

    CAMK2A-mediated pCREB is involved in Ca2+ induced expression of BDNF which is imperative for neuronal signaling and neurite outgrowth.

    “It has been shown that CAMK2A-mediated pCREB is involved in Ca2+ induced expression of BDNF which is imperative for neuronal signaling and neurite outgrowth (Yan et al., 2016).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Yan et al., 2016 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Activated microglial cells in septic animals exhibit heightened secretion of pro-inflammatory factors that result in synaptic impairment, forming cellular basis of memory and cognitive decline.

    “It has been previously reported that activated microglial cells in septic animals exhibit heightened secretion of pro-inflammatory factors that result in synaptic impairment, which forms the cellular basis of memory and cognitive decline (Moraes et al., 2015).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Moraes et al., 2015 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    miR-101 and miR-142-3p are expressed in peripheral macrophages, but their functions in microglia remain unknown.

    “are expressed in peripheral macrophages, but their functions in microglia remain unknown (Zhu et al., 2010; Xie et al., 2014).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Zhu et al., 2010 source
    • cites Xie et al., 2014 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    CAMK2A plays vital roles in synaptic plasticity, learning, and memory.

    “CAMK2A is a subunit of CAMK2 protein, which is a ubiquitous serine/threonine-protein kinase present in the brain playing vital roles in synaptic plasticity, learning, and memory (Stephenson et al., 2017).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Stephenson et al., 2017 source

      Not checked in the free run.

  • The quote only partly states this claim.

    Interpretationown data

    The CAMK2A-CREB-BDNF pathway is downregulated in LPS-activated microglia.

    “These results indicate that the CAMK2A-CREB-BDNF pathway is downregulated in activated microglia.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Ca2+ activates CAMKs, which phosphorylate CREB (pCREB), which in turn activates BDNF transcription by binding to a cAMP-response element within the gene.

    “Ca2+ acts by activating CAMKs which trigger phosphorylation of CREB (pCREB), which in turn activates BDNF transcription by binding to a cAMP-response element within the gene (Su et al., 2016; Yan et al., 2016).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites Su et al., 2016

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Yan et al., 2016 source

  • May combine two claims.

    Interpretationown data

    Loss-of-function and gain-of-function studies confirmed that miR-142-3p targets CAMK2A affecting the CAMK2A-CREB-BDNF signaling pathway in microglia.

    “Furthermore, loss-of-function and gain-of-function studies confirmed that miR-142-3p targets CAMK2A affecting the CAMK2A-CREB-BDNF signaling pathway in microglia.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Data are represented as mean ± SD from at least three independent experiments.

    “Data is represented as mean ± SD from at least three independent experiments.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Microglial activation coupled with secretion of pro-inflammatory factors in aging brain depresses LTP.

    “Moreover, microglial activation coupled with the secretion of pro-inflammatory factors in the aging brain has been shown to depress LTP (Griffin et al., 2006).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Griffin et al., 2006 source

  • May combine two claims.

    Study design and conductown data

    The efficiency of CAMK2A knockdown in microglia was confirmed by western blotting, and the shCAMK2A clone with maximal knockdown was selected.

    “The efficiency of knockdown in microglia was confirmed using western blotting analysis and the shCAMK2A clone that induced maximal knockdown was selected for further analysis.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    miR-142-3p functions as a regulator of neuroinflammation by modulating expression of proinflammatory mediators in response to different pathological stimuli.

    “Several studies have shown that miR-142-3p functions as a regulator of neuroinflammation by modulating the expression of proinflammatory mediators in response to different pathological stimuli, such as multiple sclerosis, neuropathic pain, human immunodeficiency virus (HIV) and simian immunodeficiency virus encephalitis (SIVE; Chaudhuri et al., 2013; Talebi et al., 2017; Zhang et al., 2018).”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites Chaudhuri et al., 2013 source
    • cites Talebi et al., 2017 source

      Queued — the background check reaches it, usually within a day.

    • cites Zhang et al., 2018 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    BDNF activates neuronal TrkB that regulates synaptic plasticity and modulates glutamatergic synaptic transmission in vivo and neuronal LTP.

    “BDNF has been shown to activate neuronal Tropomyosin-related kinase receptor B (TrkB) that regulates synaptic plasticity and modulate glutamatergic synaptic transmission in vivo and neuronal LTP, which is a key feature of memory formation and consolidation (Parkhurst et al., 2013; Lai et al., 2018).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Parkhurst et al., 2013 source

      Not checked in the free run.

    • cites Lai et al., 2018 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    CAMK2A is a multifunctional protein kinase critical for execution of cellular Ca2+ signal transductions and functions as a molecular substrate for LTP, forming molecular basis of learning and memory.

    “CAMK2A, which is a multifunctional protein kinase known to be critical for the execution of cellular Ca2+ signal transductions and functions as a molecular substrate for LTP, forming the molecular basis of learning and memory (Liu and Murray, 2012).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Liu and Murray, 2012 source

  • May combine two claims.

    Interpretationown data

    miR-142-3p-mediated downregulation of CAMK2A in microglia leads to repression of BDNF, which is involved in synaptic plasticity.

    “Overall, these results demonstrate that miR-142-3p-mediated downregulation of CAMK2A in microglia leads to the repression of BDNF, which is involved in synaptic plasticity.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Microglial BDNF contributes to learning-dependent synapse formation.

    “Of note, a recent study reported the significant contribution of microglial brain-derived neurotrophic factor (BDNF) towards learning-dependent synapse formation (Parkhurst et al., 2013; Saw et al., 2020).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Parkhurst et al., 2013 source

      Not checked in the free run.

    • cites Saw et al., 2020 source

      Not checked in the free run.

25 of 25

  • The paper relies on this without support.

    There are no comprehensive profiling studies of miRNA expression patterns in activated microglia.

    “Despite recent studies evaluating the role of miRNAs in microglial activation in CNS pathologies, there are no comprehensive profiling studies of miRNA expression patterns in activated microglia.”

  • The paper relies on this without support.

    The molecular and epigenetic mechanisms underlying microglia-mediated maintenance of neuronal synapses under health and diseases remain unclear.

    “However, the molecular and epigenetic mechanisms underlying microglia-mediated maintenance of neuronal synapses under health and diseases remain unclear.”

  • The paper relies on this without support.

    The shRNA-mediated knockdown of CAMK2A is specific and does not produce off-target effects that could affect BDNF.

    “Stable knockdown of CAMK2A was performed by lentiviral mediated transduction of CAMK2A specific shRNA in BV2 microglial cells.”
    “The efficiency of knockdown in microglia was confirmed using western blotting analysis and the shCAMK2A clone that induced maximal knockdown was selected for further analysis.”

  • The paper relies on this without support.

    There is a dearth of information on the miRNAs that regulate microglia-mediated synaptic maintenance.

    “While there is an adequate understanding of miRNA-mediated regulation of the inflammatory response of microglia during pathology, there is a surprising dearth of information on the miRNAs that regulate microglia-mediated synaptic maintenance.”

  • The paper relies on this without support.

    Microglial activation is a hallmark of neuroinflammation.

    “Given that microglial activation is a hallmark of neuroinflammation”
5 of 5

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • miR-7 regulates neuronal death and glutamatergic signaling; miR-137 is critical for neural development; miR-935 and miR-129-2-3p are elevated in epileptic brains and plasma.

    “miR-7 regulates neuronal death and glutamatergic signaling 40,41 ; miR-137 is critical for neural development 42 ; miR-935 and miR-129-2-3p are both elevated in epileptic brains and plasma 43 .”

    From Human brain microRNAs exhibit cell-type specificity and age dependence (2026) · cites this paper as [41]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • CAMK2 isoforms are listed inconsistently

    Minor

    The paper first identifies the four CAMK2 isoforms as a, b, d, and g, but then names c and d as two of the isoforms. The two lists disagree about whether the fourth isoform is c or g.

1 of 1

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Related

Authors
Gupta, N., Jadhav, S., Tan, K.-L., Saw, G., Mallilankaraman, K. B., & Dheen, S. T.
Affiliations
National University of Singapore (SG)
Corresponding author
Dheen, S. Thameem
ORCID
Venue
Frontiers in Cellular Neuroscience
Publisher
Frontiers Media SA
Published
2020-05-21
Volume
14
Pages
132-132
ISSN
1662-5102 (ISSN-L)
DOI
10.3389/fncel.2020.00132
PMC
PMC7253665
OpenAlex
W3027018954
Semantic Scholar
1655826ce21e81e612bda13ee7f3516231327ee0
Cited by
40
References
75
Citations by year
2026: 3 · 2025: 5 · 2024: 10 · 2023: 6 · 2022: 5 · 2021: 10 · 2019: 1
FWCI
2.11
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • National University of Singapore (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
miR-142-3p, microglial activation, CAMK2A, brain-derived neurotrophic factor, CREB phosphorylation, microRNA target regulation, lipopolysaccharide, synaptic plasticity, long-term potentiation, miRNA microarray, 3' untranslated region

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