Reuterin isolated from the probiotic Lactobacillus reuteri promotes periodontal tissue regeneration by inhibiting Cx43-mediated the intercellular transmission of endoplasmic reticulum stress.

OBJECTIVE: The present study aimed to evaluate the effects of reuterin, a bioactive isolated from the probiotic Lactobacillus reuteri (L. reuteri) on periodontal tissue regeneration, and provide a new strategy for periodontitis treatment in the future. BACKGROUND: Data discussing the present state of the field: Probiotics are essential for maintaining oral microecological balance. Our previous study confirmed that probiotic L. reuteri extracts could rescue the function of mesenchymal stem cells (MSCs) and promote soft tissue wound healing by neutralizing inflammatory Porphyromonas gingivalis-LPS. Periodontitis is a chronic inflammatory disease caused by bacteria seriously leading to tooth loss. In this study, we isolated and purified reuterin from an extract of L. reuteri to characterize from the extracts of L. reuteri to characterize its role in promoting periodontal tissue regeneration and controlling inflammation in periodontitis. METHODS: Chromatographic analysis was used to isolate and purify reuterin from an extract of L. reuteri, and HNMR was used to characterize its structure. The inflammatory cytokine TNFα was used to simulate the inflammatory environment. Periodontal ligament stem cells (PDLSCs) were treated with TNFα and reuterin after which their effects were characterized using scratch wound cell migration assays to determine the concentration of reuterin, an experimental periodontitis model in rats was used to investigate the function of reuterin in periodontal regeneration and inflammation control in vivo. Real-time PCR, dye transfer experiments, image analysis, alkaline phosphatase activity, Alizarin red staining, cell proliferation, RNA-sequencing and Western Blot assays were used to detect the function of PDLSCs. RESULTS: In vivo, local injection of reuterin promoted periodontal tissue regeneration of experimental periodontitis in rats and reduced local inflammatory response. Moreover, we found that TNFα stimulation caused endoplasmic reticulum (ER) stress in PDLSCs, which resulted in decreased osteogenic differentiation. Treatment with reuterin inhibited the ER stress state of PDLSCs caused by the inflammatory environment and restored the osteogenic differentiation and cell proliferation functions of inflammatory PDLSCs. Mechanistically, we found that reuterin restored the functions of inflammatory PDLSCs by inhibiting the intercellular transmission of ER stress mediated by Cx43 in inflammatory PDLSCs and regulated osteogenic differentiation capacity. CONCLUSION: Our findings identified reuterin isolated from extracts of the probiotic L. reuteri, which improves tissue regeneration and controls inflammation, thus providing a new therapeutic method for treating periodontitis.

The impacts of oral and gut microbiota on alveolar bone loss in periodontitis.

Periodontitis, a chronic infectious disease, primarily arises from infections and the invasion of periodontal pathogens. This condition is typified by alveolar bone loss resulting from host immune responses and inflammatory reactions. Periodontal pathogens trigger aberrant inflammatory reactions within periodontal tissues, thereby exacerbating the progression of periodontitis. Simultaneously, these pathogens and metabolites stimulate osteoclast differentiation, which leads to alveolar bone resorption. Moreover, a range of systemic diseases, including diabetes, postmenopausal osteoporosis, obesity and inflammatory bowel disease, can contribute to the development and progression of periodontitis. Many studies have underscored the pivotal role of gut microbiota in bone health through the gut-alveolar bone axis. The circulation may facilitate the transfer of gut pathogens or metabolites to distant alveolar bone, which in turn regulates bone homeostasis. Additionally, gut pathogens can elicit gut immune responses and direct immune cells to remote organs, potentially exacerbating periodontitis. This review summarizes the influence of oral microbiota on the development of periodontitis as well as the association between gut microbiota and periodontitis. By uncovering potential mechanisms of the gut-bone axis, this analysis provides novel insights for the targeted treatment of pathogenic bacteria in periodontitis.

Antimicrobial peptides in treatment of Stage III Grade B periodontitis: A randomized clinical trial.

BACKGROUND: To evaluate the effects of antimicrobial peptides (AMPs) on Stage III Grade B periodontitis. METHODS: This trial abided by the principle of consistency test, approved by ethics committee and registered in clinical trials. All qualified 51 patients with Stage III Grade B periodontitis were randomly divided into three groups: SRP group, SRP with minocycline hydrochloride (Mino group) as Control groups, and SRP with AMPs (AMP group) as the Test group. Clinical examinations and subgingival plaques were monitored at baseline and at 7 and 90 days after treatment in the SRP, SRP with AMP and Mino groups. RESULTS: The AMP group (Test group) had a reduced PD (Periodontal probing depth) and an attachment gain significantly higher than SRP and Mino groups (Control groups) at day 90. The abundance of periodontal pathogens was decreased in the AMP group at 7 and 90 days compared with the SRP group and Mino group. Only the AMP group showed an increase the abundance of periodontal probiotics including Capnocytophaga, Gemella, and Lactobacillus at 7 and 90 days. CONCLUSIONS: This study shows that AMPs as an adjunct to SRP promote additional clinical and microbiological benefits in the treatment of Stage III Grade B periodontitis.

Strong Second Harmonic Generation from Bilayer Graphene with Symmetry Breaking by Redox-Governed Charge Doping.

Missing second-order nonlinearity in centrosymmetric graphene overshadows its intriguing optical attribute. Here, we report redox-governed charge doping could effectively break the centrosymmetry of bilayer graphene (BLG), enabling a strong second harmonic generation (SHG) with a strength close to that of the well-known monolayer MoS2. Verified from control experiments with in situ electrical current annealing and electrically gate-controlled SHG, the required centrosymmetry breaking of the emerging SHG arises from the charge-doping on the bottom layer of BLG by the oxygen/water redox couple. Our results not only reveal that charge doping is an effective way to break the inversion symmetry of BLG despite its strong interlayer coupling but also indicate that SHG spectroscopy is a valid technique to probe molecular doping on two-dimensional materials.

Regulation of the Host Immune Microenvironment in Periodontitis and Periodontal Bone Remodeling.

The periodontal immune microenvironment is a delicate regulatory system that involves a variety of host immune cells including neutrophils, macrophages, T cells, dendritic cells and mesenchymal stem cells. The dysfunction or overactivation of any kind of local cells, and eventually the imbalance of the entire molecular regulatory network, leads to periodontal inflammation and tissue destruction. In this review, the basic characteristics of various host cells in the periodontal immune microenvironment and the regulatory network mechanism of host cells involved in the pathogenesis of periodontitis and periodontal bone remodeling are summarized, with emphasis on the immune regulatory network that regulates the periodontal microenvironment and maintains a dynamic balance. Future strategies for the clinical treatment of periodontitis and periodontal tissue regeneration need to develop new targeted synergistic drugs and/or novel technologies to clarify the regulatory mechanism of the local microenvironment. This review aims to provide clues and a theoretical basis for future research in this field.

Increased levels of PD1 and glycolysis in CD4+ T cells are positively associated with lymph node metastasis in OSCC.

BACKGROUND: Cervical lymph node metastasis is one of the poorest prognostic factors in oral squamous cell carcinoma (OSCC). Activated immune cells generally have metabolic abnormalities in the tumour microenvironment. However, it is unknown whether abnormal glycolysis in T cells could facilitate metastatic lymph nodes in OSCC patients. The aim of this study was to investigate the effects of immune checkpoints in metastatic lymph nodes and determine the correlation between glycolysis and immune checkpoint expression in CD4+ T cells. METHODS: Flow cytometry and immunofluorescence staining were used to analyse the differences in CD4+ PD1+ T cells between metastatic lymph nodes (LN+) and negative lymph nodes (LN-). RT‒PCR was performed to detail the expression of immune checkpoints and glycolysis-related enzymes in LN+ and LN-. RESULTS: The frequency of CD4+ T cells decreased in LN+ patients (p = 0.0019). The PD1 expression of LN+ increased markedly compared to that of LN- (p = 0.0205). Similarly, the PD1 of CD4+ T cells in LN+ increased significantly compared to that of LN-. Additionally, glycolysis-related enzyme levels in CD4+ T cells from LN+ patients were dramatically higher than those in LN- patients. PD1 and Hk2 expression in CD4+ T cells was also increased in LN+ OSCC patients with prior surgical treatment compared to those without. CONCLUSIONS: These findings suggest that lymph node metastasis and recurrence in OSCC are associated with increases in PD1 and glycolysis in CD4+ T cells; this response may serve as a potential regulator of OSCC progression.

MicroRNA-155 targets SOCS1 to inhibit osteoclast differentiation during orthodontic tooth movement.

BACKGROUND: MicroRNA-155 (miR-155) is a multifunctional miRNA whose expression is known to be involved in a range of physiological and pathological processes. Its association with several oral diseases has been established. However, the specific role of miR-155 in orthodontic tooth movement remains unclear. In this study, we investigated the impact of miR-155 on osteoclast differentiation and orthodontic tooth movement models, aiming to explore the underlying mechanisms. METHODS: In this experiment, we utilized various agents including miR-155 mimic, miR-155 inhibitor, as well as non-specific sequences (NC mimic & NC inhibitor) to treat murine BMMNCs. Subsequently, osteoclast induction (OC) was carried out to examine the changes in the differentiation ability of monocytes under different conditions. To assess these changes, we employed RT-PCR, Western blotting, and TRAP staining techniques. For the orthodontic tooth movement model in mice, the subjects were divided into two groups: the NaCl group (injected with saline solution) and the miR-155 inhibitor group (injected with AntagomiR-155). We observed the impact of orthodontic tooth movement using stereoscopic microscopy, micro-CT, and HE staining. Furthermore, we performed RT-PCR and Western blotting analyses on the tissues surrounding the moving teeth. Additionally, we employed TargetScan to predict potential target genes of miR-155. RESULTS: During osteoclast induction of BMMNCs, the expression of miR-155 exhibited an inverse correlation with osteoclast-related markers. Overexpression of miR-155 led to a decrease in osteoclast-related indexes, whereas underexpression of miR-155 increased those indexes. In the mouse orthodontic tooth movement model, the rate of tooth movement was enhanced following injection of the miR-155 inhibitor, leading to heightened osteoclast activity. TargetScan analysis identified SOCS1 as a target gene of miR-155. CONCLUSIONS: Our results suggest that miR-155 functions as an inhibitor of osteoclast differentiation, and it appears to regulate osteoclasts during orthodontic tooth movement. The regulatory mechanism of miR-155 in this process involves the targeting of SOCS1.

HPRT promotes proliferation and metastasis in head and neck squamous cell carcinoma through direct interaction with STAT3.

Increasing effort has been put into finding novel molecular pathways to improve the efficiency of EGFR inhibitors against head and neck squamous cell cancer (HNSCC). In this study, we performed data mining and bioinformatically analysed RNA-Seq data downloaded from TCGA and confirmed that higher expression of HPRT in HNSCC tissue was related to poor prognosis of patients. Then, we conducted in vitro and in vivo loss- and gain-of-function experiments to demonstrate the role of HPRT in HNSCC cell lines. Overexpression of HPRT increased the gene expression of epithelial mesenchymal transition markers via direct interaction with STAT3. Knocking down HPRT significantly decreased tumour growth and enhanced the anticancer effect of EGFR inhibitors against HNSCC xenografts. In conclusion, HPRT is a binding partner of STAT3 that promotes EMT and proliferation. Our findings support HPRT as a promising prognostic indicator and potential therapeutic target for HNSCC.

Machine Learning Driven Synthesis of Few-Layered WTe2 with Geometrical Control.

Reducing the lateral scale of two-dimensional (2D) materials to one-dimensional (1D) has attracted substantial research interest not only to achieve competitive electronic applications but also for the exploration of fundamental physical properties. Controllable synthesis of high-quality 1D nanoribbons (NRs) is thus highly desirable and essential for further study. Here, we report the implementation of supervised machine learning (ML) for the chemical vapor deposition (CVD) synthesis of high-quality quasi-1D few-layered WTe2 NRs. Feature importance analysis indicates that H2 gas flow rate has a profound influence on the formation of WTe2, and the source ratio governs the sample morphology. Notably, the growth mechanism of 1T' few-layered WTe2 NRs is further proposed, which provides new insights for the growth of intriguing 2D and 1D tellurides and may inspire the growth strategies for other 1D nanostructures. Our findings suggest the effectiveness and capability of ML in guiding the synthesis of 1D nanostructures, opening up new opportunities for intelligent materials development.

Suppressing Water Dissociation via Control of Intrinsic Oxygen Defects for Awakening Solar H2 O-to-H2 O2 Generation.

BiVO4 theoretically has a thermodynamic activity trend toward highly selective water oxidative H2 O2 formation, but it is more inclined to generate O2 in practical. The influence of intrinsic oxygen vacancy (Ovac ), especially, on surface reactivity, has never been considered as a possible activity loss mechanism in the synthetic BiVO4 . In this work, it is theoretically and experimentally demonstrated that the intrinsic surface Ovac is responsible for lower H2 O2 evolution activity via promoting water dissociation to form intermediate. Through an annealing process under a V2 O5 rich atmosphere, the surface Ovac can be eliminated that awakens the photoelectrochemical (PEC) water oxidative H2 O2 activity in a NaHCO3 electrolyte, which achieves an average of 58.4%, and increases by up to 4.28 times of the one annealed in air. This work offers a general understanding of catalytic activity loss and may be extended to other photo or electrocatalysts for catalytic selectivity regulation.

Expression profile of circular RNA and construction of circular RNA-Micro RNA network in salivary adenoid cystic carcinoma.

BACKGROUND: Circular RNAs (circRNAs) is a newly discovered type of non-coding RNA, the abnormal expression of which has been demonstrated in many types of human tumors. So they have been considered as promising candidates as diagnostic and therapeutic targets in cancer. This research aimed to screen the profile of circRNA expression in salivary adenoid cystic carcinoma (SACC). METHODS: Using the threshold of FDR < 0.05 and fold change > 2 or < 0.5, 5 up-regulated and 26 down-regulated circRNAs were identified. The reliability of sequencing was verified by the expression detection of randomly selected circRNAs via qRT-PCR. RESULTS: Moreover, the circRNA-miRNA system was established by bioinformatics approaches and successfully identified an interaction between circRNA ABCA13 and a cancer-related miRNA (miR-138-5p), which was also verified by qRT-PCR. Moreover, the predicted molecular interaction proved that circRNA ABCA13 may promote SACC through inhibition of miR-138-5p. CONCLUSIONS: Collectively, this study has offered the first report about the circRNA expression profile and circRNA-miRNA network in SACC. All of the above could benefit the exploration of novel therapeutic target in SACC treatment.

Increased Th17 and Th22 Cell Percentages Predict Acute Lung Injury in Patients with Sepsis.

PURPOSE: This study was conducted to investigate the percentages of Th22 and Th17 cells in the peripheral blood of septic patients with and without acute lung injury (ALI) and their clinical significance. METHODS: A total of 479 patients were divided into non-ALI and ALI groups. The percentages of Th22 and Th17 cells and the levels of interleukin 22 (IL-22), 6 (IL-6), and 17 (IL-17) were determined. Receiver operating characteristic curve analysis was performed to assess the diagnostic value of Th22 and Th17 cells to predict sepsis-induced ALI. RESULTS: The lung injury prediction score (LIPS), IL-6, IL-17, and IL-22 levels and the percentages of Th17 and Th22 cells were significantly higher in the ALI group (P < 0.05). They were significant factors affecting sepsis-induced ALI (P < 0.05). Multivariate logistic regression analysis showed that the LIPS (OR = 1.130), IL-17 (OR = 1.982), IL-22 (OR = 2.612) and the percentages of Th17 (OR = 2.211) and Th22 (OR = 3.230) cells were independent risk factors for ALI. The area under the curve of Th22 cells was 0.844 to predict ALI with a cutoff value of 6.81%. The sensitivity and specificity for early diagnosis of sepsis-induced ALI by the Th22 cell percentage were 78.72% and 89.13%, respectively. CONCLUSIONS: Th22 and Th17 cells in peripheral blood are significantly increased in septic patients with ALI and they may be used as biomarkers for early diagnosis of sepsis-induced ALI.

SFRP2 promotes stem cells from apical papilla-mediated periodontal tissue regeneration in miniature pig.

Mesenchymal stem cell-based therapy is a reliable treatment for periodontal tissue regeneration, while ideal regeneration rate is still a facing problem. In previous study, we found SFRP2 a promising gene in modulating mesenchymal stem cells potential. We further investigated its role on periodontal tissue regeneration. We created periodontitis model in miniature pigs and locally injected with stem cells from apical papilla (SCAP). The periodontitis models were classed into three groups, SFRP2-SCAP group (injected with SCAP overexpressing with SFRP2), SCAP group (injected with SCAP transduced with vector backbone) and saline group (vehicle group injected with saline). Clinical assignment, CT scanning, histopathological assessment and quantitative analysis were applied to evaluate the regeneration effect. Twelve weeks after the injection, we found healthier gingival status in SFRP2-SCAP group than the other two groups. Clinical assignment results showed values of probing depth, gingival recession and attachment loss were improved in SFRP2-SCAP group than that of SCAP group and saline group. The volume of newborn bone was also enhanced in SFRP2-SCAP group than SCAP group and saline group. The difference of clinical assignments and newborn bone between each group was significant relevant. HE staining demonstrated increased tissue regeneration in SFRP2-SCAP group than SCAP group and saline group. Our findings revealed that SFRP2 could enhance SCAP-mediated periodontal tissue regeneration and provide a potential target for improving the regeneration of periodontal tissue.

Screening and bioinformatics analysis of mRNA, long non-coding RNA and circular RNA expression profiles in mucoepidermoid carcinoma of salivary gland.

Mucoepidermoid carcinoma (MEC) of salivary gland is a disease characterized by high rate of diatant metastasis, and associated with poor outcomes. However, the molecular mechanisms underlying the MEC remain poorly understand. Here, we simultaneously detected, for the first time, the expression profiles of mRNAs, lncRNAs, and circRNAs in four pairs of MEC and matched non-carcinoma tissues by microarrays. A total of 3612 mRNA, 3091 lncRNAs, and 284 circRNAs were altered during the pathogenesis of MEC. The functions of these differentially expressed RNAs were predicted by Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Co-expression networks of lncRNA-mRNA and circRNA-miRNA were conducted to uncovered the hidden ceRNA mechanisms. Moreover, NONHSAT154433.1 that associated with ADAM12 and hsa_circ_0012342 were further screened and confirmed using qRT-PCR analysis. In conclusion, this study provides a systematic perspective on the potential function of non-coding RNAs (ncRNAs) in the molecular mechanisms of MEC. Among these, NONHSAT154433.1 and hsa_circ_0012342 might be served as potential prognostic biomarkers and therapeutic target of MEC.

The miR-3940-5p inhibits cell proliferation of gingival mesenchymal stem cells.

OBJECTIVES: Drug-induced gingival overgrowth (DIGO) is a well-recognized side effect of nifedipine (NIF). However, the molecular mechanisms of DIGO are still unknown. Here, we explored the possible role of miR-3940-5p in DIGO using NIF-treated gingival mesenchymal stem cells (GMSCs). MATERIAL AND METHODS: CFSE and cell cycle assays were used to examine cell proliferation. The alkaline phosphatase (ALP) activity assay, Alizarin Red staining, quantitative calcium analysis, and osteogenesis-related gene expression were used to examine osteo/dentinogenic differentiation. RESULTS: The CFSE assay showed that NIF enhanced cell proliferation, and the over-expression of miR-3940-5p inhibited the proliferation of GMSCs with or without NIF stimulation. Cell cycle assays revealed that the cell cycle was arrested at the G0/G1 phase. Furthermore, it was found that the over-expression of miR-3940-5p upregulated p15INK4b , p18INK4c , p19INK4d , and Cyclin A and downregulated Cyclin E in GMSCs with or without NIF treatment. In addition, the over-expression of miR-3940-5p enhanced ALP activity and mineralization in vitro and increased the expression of the osteo/dentinogenic differentiation markers DSPP and DMP1 and the key transcription factor DLX5 in GMSCs. CONCLUSIONS: miR-3940-5p inhibited cell proliferation, enhanced the osteo/dentinogenic differentiation of GMSCs, and might play a role in DIGO as a potent agent in the treatment of nifedipine-induced gingival overgrowth.

Epiregulin promotes the migration and chemotaxis ability of adipose-derived mesenchymal stem cells via mitogen-activated protein kinase signaling pathways.

To investigate the function of epiregulin (EREG) in the migration and chemotaxis ability of mesenchymal stem cells. Adipose-derived stem cells (ADSCs) were used in this investigation. Lentiviral EREG short hairpin RNA was applied to silence EREG expression in ADSCs. Human recombinant EREG protein (rhEREG) was used to perform a gain-of-function study. Scratch-simulated wound migration and transwell chemotaxis assays were used to examine the migration and chemotaxis capacity of ADSCs in vitro. Using a Western blot assay, the expressions of p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinases 1 and 2 (Erk1/2), and protein kinase B were detected. Depletion of EREG caused by specific short hairpin RNA restrained the migration and chemotaxis ability of ADSCs and inhibited the expressions of phosphorylated p38 MAPK, JNK, and Erk1/2. rhEREG improved ADSCs migration and chemotaxis capacity, which was repressed by knockdown of EREG and rescued the expressions of phosphorylated p38 MAPK, JNK, and Erk1/2 impaired by silencing EREG. Furthermore, rhEREG-improved migration and chemotaxis ability in EREG-depleted-ADSCs was restricted by a specific inhibitor, SB203580, for blocking p38 MAPK signaling, PD98059 for blocking Erk1/2 signaling, or SP600125 for blocking JNK signaling in ADSCs separately. EREG promotes migration and chemotaxis ability of ADSCs through MAPK signaling pathways.

Homeobox C10 inhibits the osteogenic differentiation potential of mesenchymal stem cells.

PURPOSE: Mesenchymal stem cells (MSCs) are a reliable cell source for tissue regeneration. However, the molecular mechanisms underlying the directed differentiation of MSCs remain unclear which impedes potential clinical applications. Recent studies have discovered that Homeobox (HOX) genes are involved in the differentiation regulation of MSCs and bone formation. In this study, we investigate the HOXC10 function in the osteogenic differentiation potential of MSCs. MATERIALS AND METHODS: Stem cells from apical papilla (SCAPs) and adipose-derived stem cells (ADSCs) were used in this study. Alkaline phosphatase (ALP) activity assays, ALP staining, Alizarin red staining, quantitative calcium analysis, osteogenesis-associated gene expression, and in vivo transplantation experiments were used to study osteogenic differentiation potential. RESULTS: Our results showed that overexpression of HOXC10 in SCAPs inhibited ALP activity and mineralization in vitro and decreased the mRNA expression of collagen alpha-1 (I) chain, bone sialoprotein, osteocalcin, and a key transcription factor, runt-related transcription factor 2, in SCAPs. Depletion of HOXC10 promoted osteogenic differentiation in SCAPs in vitro. In addition, in vivo transplantation experiments in nude mice confirmed that SCAPs osteogenesis was triggered when HOXC10 was downregulated. Furthermore, depletion of HOXC10 also enhanced osteogenic differentiation in ADSCs. CONCLUSIONS: Taken together, these results indicated that HOXC10 decreased the MSC osteogenic differentiation potential. Thus, inhibition of HOXC10 in MSCs might have the potential to improve tissue regeneration and provide insight into the mechanism underlying the directed differentiation of MSCs.

Unique Transformation from Graphene to Carbide on Re(0001) Induced by Strong Carbon-Metal Interaction.

During graphene growth on various transition metals in the periodic table, metal carbides always emerge to behave as complex intermediates. On VIII metals, metastable carbides usually evolve and then transform into graphene along the phase interfaces, and even no metal carbides can form on IB-IIB metals. In contrast, during graphene growth on group IVB-VIB metals, carbides are usually generated even before the evolution of graphene and stably exist throughout the whole growth process. However, for the remaining transition metals, e.g., group VIIB, located in between IVB-VIB and VIII, the interplay between graphene and carbide is still vague. Herein, on Re(0001) (VIIB), we have revealed a novel transition from graphene to metal carbide (reverse to that on VIII metals) for the first time. This transition experienced graphene decomposition, dissolution, and carbon segregation processes, as evidenced by scanning tunneling microscopy (STM) and on-site, variable-temperature low electron energy diffraction (LEED) characterizations. This work thus completes the picture about the interplay between graphene and carbide on/in transition metals in the periodic table, as well as discloses a new territory for the growth of carbon-related materials, especially the metal carbide.

A giant intrinsic photovoltaic effect in atomically thin ReS2.

The photovoltaic (PV) effect in non-centrosymmetric materials consisting of a single component under homogeneous illumination can exceed the fundamental Shockley-Queisser limit compared to the traditional p-n junctions. Two-dimensional (2D) materials with a reduced dimensionality and smaller bandgap were predicated to be better candidates for the PV effect with high efficiency exceeding that of traditional ferroelectric perovskite oxides. Here, we report the giant intrinsic PV effect in atomically thin rhenium disulfide (ReS2) with centrosymmetry breaking. In graphene/ReS2/graphene sandwich structures, significant short-circuit currents (Isc) were observed with illumination over the visible spectral range, presenting the highest responsivity (110 mA W-1) and external quantum efficiency (25.7%) among those reported PV effects in 2D materials. This giant PV effect could be ascribed to the spontaneous-polarization induced depolarization field in even-number-layered ReS2 flakes benefiting from the distorted 1T lattice structure. Our results provide a new potential candidate material for the development of novel high-efficiency, miniaturized and easily integrated photodetectors and solar cells.