and Periodontitis: A Source of Connection to Systemic Diseases

miRNA

Regulation periodontally affected tissues

Type of immune system affected in periodontitis

Mechanism

Upregulated

Downregulated

miR-30e

Yes

Innate immune system

Inhibits NK cell activation. This downregulation increases NK cell activation and hence increases tissue destruction

miR-31

Yes

Innate immune system

Negative regulator of NF-κB and mediates osteoclastogenesis. Its downregulation produces over-activation of TLRs and decreases bone formation

miR-146a

Yes

Innate and adaptive immune system

Regulates NF-κB signaling pathway activation, reduces dendritic cell cytokine production, impairs dendritic cell TLRs, and controls B-cell development

miR-148a

Yes

Innate and adaptive immune system

Impairs antigen presentation function by dendritic cells and the whole innate response

miR-155

Yes

Innate and adaptive immune system

Regulates NF-κB signaling pathway, mediates type I interferon and interferon-gamma production; increases TLR sensitivity, critical in dendritic cell maturation; controls CD8 T-cell response; and indirectly influences the activation of T-helper cell 17

miR-200a

Yes

Innate immune system

Negative regulation of IL-12 in NK cells. Thus, its downregulation causes increased production

miR-210

Yes

Adaptive immune system

Its downregulation increases T-cell signaling

miR-451

Yes

Innate immune system

Suppression of neutrophil chemotaxis

miR-486

Yes

Innate immune system

Increases exponentially NF-κB signaling pathway

miR-650

Yes

Adaptive immune system

Regulates B-cell proliferation

Table 3.2

Main lncRNAs in periodontally affected gingival tissues

lncRNA

Regulation periodontally affected tissues

Type of immune system affected in periodontitis

Mechanism

Upregulated

Downregulated

HOTAIR

 

Yes

Still unknown

RP3-461P17

RP1-300I2.2

Yes

Still unknown

TIRAP

Yes

Still unknown

CDKN2A

Yes

Still unknown

CDKN2B

Yes

Still unknown

lincRNA-CDON-1

Yes

Innate immune system

Affects signaling pathways of TLR activation

ANRIL

Yes

 

Regulation of chromatin, ADIPOR1, VAMP3, and C11ORF10 expression. Its downregulation provokes reduced expression of those markers, increasing the risk of atherosclerosis, metabolic syndrome, periodontitis, and several forms of cancer

Table 3.3

Some examples of methylations in cancer expression

Author/year

Country

Type of cancer involved

Epigenetic modification

Results

Mechanism

Upregulation of cancer

Downregulation of cancer

[94]

Belgium

Melanoma

DNMT1

Yes

Yes

Transient depletion of DNMT1 can lead to long-term activation of cancer-germline genes and repression of mitosis/division-related genes at the same time

[95]

USA

Colon cancer

DNMT1

Yes

Interaction between a subset of lncRNAs and DNMT1 was reduced in colon cancer cells, which contributes to aberrant DNA methylation and gene expression in tumorigenesis

[96]

USA

Lung cancer

DNMT1

Yes

There is a cross talk between tyrosine-protein kinase KIT and DNMT1 in the development of drug resistance, which implies an upregulation of oncogenesis process by means of that interaction

[97]

China

Breast cancer

DNMT1

Yes

DNMT1, DNMT3A, and DNMT3B commonly or individually contributed to DNA methylation in different breast cancer cells

Table 3.4

Some examples of histone acetylations in cancer expression

Author/year

Country

Type of cancer involved

Epigenetic modification

Results

Mechanism

Upregulation of cancer

Downregulation of cancer

[98]

China

Hepatocellular carcinoma

Histone acetylation

Yes

Histone deacetylase (HDAC) 9 increased the expression of miR-376a by upregulating the global histone H3K18 acetylation level, which is inversely correlated with hepatocellular carcinoma

[99]

Poland

Colorectal cancer

Histone acetylation

Yes

Histone H3 lysine 27 acetylation (H3K27Ac) is upregulated in CRC

[100]

Germany

Lymphoma, hepatoma,

Histone acetylation

Yes

The 5-HTT gene is epigenetically downregulated by histone deacetylation. The 5-HTT gene is usually silenced in several types of cancer

Table 3.5

Some examples of miRNAs and lncRNAs in cancer expression

Author/year

Country

Type of cancer involved

Epigenetic modification

Results

Mechanism

Upregulation of Cancer

Downregulation of Cancer

[90]

USA

Pancreatic cancer

miR-31

Yes

Expression of enforced miR-31 significantly enhanced invasion and migration of multiple pancreatic cancer cells

[89]

Taiwan

Oral potentially malignant disorder

miR-31

Yes

Epithelial dysplasia and miR-31 upregulation synergistically predict the increased incidence of recurrence and/or malignant transformation in patients with OPMD. Detection of miR-31 expression is an adjuvant method for screening of high-risk OPMD

[91]

Germany

Head and neck squamous cell carcinoma

miR-146a and miR-155

Yes

Downregulation of miR-146a and miR-155 in blood of patients correlated with the occurrence of distant metastasis regarding tumor patients

[93]

China

Oral squamous cell carcinoma

Long noncoding RNA-HOX transcript antisense intergenic RNA (HOTAIR)

Yes

HOTAIR was highly expressed in OSCC tissues and facilitated the growth of OSCC cells, thus probably being an eligible molecular marker for OSCC diagnosis and prognosis determination

[93]

 

Oral squamous cell carcinoma

Long noncoding RNA-HOX transcript antisense intergenic RNA (HOTAIR)

Yes

Overexpression of HOTAIR indicated poor overall survival in OSCC patients. Knockdown of HOTAIR in OSCC cells decreased cell proliferation and colony formation, increased cell invasion and migration, and induced apoptosis in vitro

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Aug 25, 2019 | Posted by in General Dentistry | Comments Off on and Periodontitis: A Source of Connection to Systemic Diseases
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