缺血预适应对大鼠肢体缺血/再灌注后肺损伤的影响

目的:观察肢体缺血预适应对大鼠肢体缺血/再灌注(I/R)后肺损伤的影响并探讨其机制。方法:将雄性Wistar大鼠随机分为4组(n=8):对照组(C),肢体缺血/再灌注组(LI/R),缺血预适应组(IPC)和L-NAME组。各组大鼠均于肢体缺血4h再灌注4h处死,分别测定其动脉血氧分压(PaO2)和二氧化碳分压(PaCO2),血浆及肺组织丙二醛(MDA)、一氧化氮(NO)、内皮素(ET)含量,计算血浆NO/ET比值;以及肺湿干比(W/D)、肺系数(LI),肺组织髓过氧化物酶(MPO)含量。结果:大鼠LI/R后4h,PaO2明显降低;W/D、LI、血浆及肺组织的MDA、NO、ET和肺组织MPO活性均明显增加,而血浆NO/ET比值明显减小。与LI/R组比较,IPC组各项损伤指标明显减轻,NO水平升高,血浆NO/ET比值明显增大。与对照组和IPC组比较,L-NAME处理组,各项损伤指标数值明显增加,NO水平降低;血浆NO/ET比值明显减小,差异均具有显著性。各组大鼠PaCO2的变化无显著性。结论:缺血预适应对肢体缺血/再灌注后肺损伤具有保护作用,其机制可能与内源性NO合成增加有关。     

地塞米松与硫酸镁对大鼠小肠缺血再灌注损伤的作用及机制

目的研究地塞米松和硫酸镁对大鼠小肠缺血再灌注（I/R）损伤的保护作用,并初步探讨其机制。方法制作小肠I/R模型,实验分为假手术阴性对照组、I/R组、硫酸镁治疗组、地塞米松治疗组、地塞米松和硫酸镁联合治疗组,比较五组血浆二胺氧化酶（DAO）、丙二醛（MDA）的含量,同时比较小肠的病理切片观察治疗效果。结果①I/R组小肠组织病理变化明显,血浆DAO、MDA比假手术阴性对照组显著升高;②硫酸镁治疗组和地塞米松治疗组小肠病理变化减轻,血浆DAO、MDA比I/R组显著降低,且两组无显著差别;③硫酸镁和地塞米松合用组的血浆MDA比I/R组显著升高,但是小肠病理变化和I/R组相比无明显区别,血浆DAO也和I/R组无明显差别。结论硫酸镁,地塞米松分别对大鼠小肠缺血再灌注有保护作用而二者合用却无明显的保护作用。     

缺血预适应对大鼠肢体缺血/再灌注后小肠细胞凋亡的影响

目的：观察大鼠肢体缺血再灌注后小肠粘膜自由基及钙含量改变与细胞凋亡情况．以及缺血预适应对其变化的影响。方法：将雄性Wistar大鼠18只,随机分为对照（Control）组,缺血／再灌注（I／R）组和缺血预适应（IPC＋I／R）组,分别测定血浆和小肠组织超氧化物歧化酶（SOD）、黄嘌呤氧化酶（XOD）、丙二醛（MDA）的含量,小肠组织钙及线粒体钙含量;小肠组织的Bel-2和Bax蛋白的表达水平;检测小肠细胞凋亡情况。结果：肢体I／R后血浆和小肠粘膜SOD减少而XOD和MDA增加;小肠组织钙及线粒体钙含量增多;Bel-2蛋白表迭和Bax表达增多,但Bel-2／Bax比值降低;凋亡细胞增多。IPC减轻了I／R后引起的XOD、MDA含量的升高,并且增加了SOD的含量;减轻了组织和线粒体钙超载;Bel-2的表达则明显升高而Bax表达较I／R组明显减少,Bel-2／Bax比值升高;凋亡细胞减少。结论：肢体IR引起小肠粘膜自由基的增多,钙超栽,凋亡细胞增多;IPC可能通过减少自由基的产生及钙超载,抑制细胞凋亡而对肢体I／R继发的小肠功能损伤起保护作用。     

胰高血糖素样肽-2对小鼠小肠缺血/再灌注损伤的保护作用

目的:观察胰高血糖素样肽-2(GLP-2)对缺血/再灌注损伤小鼠小肠的保护效应.方法:采用肠缺血/再灌注(I/R)模型,将32只小鼠随机分为4组(n=8)假手术(Sham)组、I/R组、I/R GLP-2保护组和I/R 谷氨酰胺(GLN)阳性对照组.光镜观察小肠黏膜形态学改变.检测小肠绒毛高度和隐窝深度;小肠组织二胺氧化酶(DAO)活性;肠系膜淋巴结(MLN)细菌易位率.结果:与假手术组相比,I/R组部分小肠绒毛坏死脱落,绒毛高度下降,隐窝变浅(P＜0 01);小肠组织DAO活性降低(P＜0.01);MLN细菌易位率增加(P＜0.05).与I/R组比,GLP-2组肠绒毛损害明显减轻,DAO活性回升(P＜0.01),细菌易位率回降(P＜0.05).结论:GLP-2对缺血/再灌注损伤小鼠小肠的形态结构及肠屏障功能具有保护作用.     

牛磺酸对大鼠肢体缺血/再灌注后肺损伤时磷脂酶A2的影响

目的:探讨牛磺酸对大鼠肢体缺血/再灌注后肺损伤时磷脂酶A2(PLA2)的影响。方法:实验采用大鼠肢体缺血/再灌注损伤模型,将Wistar大鼠30只随机分为3组(n=10),对照组(control)、单纯缺血/再灌注组(I/R)、牛磺酸 缺血/再灌注组(Tau I/R),分别测定血浆丙二醛(MDA)、黄嘌呤氧化酶(XOD)、超氧化物歧化酶(SOD)以及肺组织Taurine、XOD、SOD、MDA、髓过氧化物酶(MPO)的含量、肺湿/干比值(W/D)和磷脂酶A2(PLA2)的活性。结果:口服牛磺酸可有效地降低肺组织MPO、PLA2和XOD的活性。结论:牛磺酸对大鼠肢体缺血再灌注后肺损伤具有保护作用,其机制之一可能与降低PLA2活性和抑制炎症反应有关。     

左旋硝基精氨酸对肺缺血预处理的抗缺血/再灌注损伤作用的影响

目的:观察一氧化氮合酶(NOS)阻滞剂左旋硝基精氨酸(L-NNA)对肺缺血预处理的影响,探讨NOS在肺缺血预处理效应中的作用.方法:40只日本大耳兔随机分成假手术(S)组,缺血/再灌注组(I/R组),缺血预处理组(IPC组)和左旋硝基精氨酸组(LNNA组),观察各组血浆丙二醛(MDA)含量、超氧歧化酶(SOD)活力,肺组织湿干重比(W/D),肺损伤定量评价指标(IQA),肺组织NOS活力以及肺组织超微结构变化.结果:IPC组与I/R组比较,MDA、W/D、IQA下降(P＜0.05或P＜0.01),SOD活力上升(P＜0.05),总NOS(TNOS)、原生型NOS(cNOS)活性明显增高(P＜0.05),电镜下肺组织损伤较轻;而预先用L-NNA(LNNA组)后使上述改变发生逆转.结论:左旋硝基精氨酸可以拮抗肺缺血预处理的抗缺血再灌注损伤作用;NOS可能是介导肺IPC效应的重要酶蛋白.     

缺血预处理对大鼠肺缺血/再灌注损伤的保护作用

目的 :观察缺血预处理 (IPC)对大鼠肺缺血 /再灌注 (I/R)损伤的保护作用 ,并初步探讨其作用机制。方法 :建立离体大鼠肺灌流模型 ,36只wistar大鼠随机分为对照组、I/R组和IPC组 ,处理完毕后分别测定平均肺动脉压(MPAP)、肺组织湿 /干重比、支气管肺泡灌洗液中肺表面活性物质磷脂及表面张力改变 ,肺组织标本送电镜检查。结果 :①电镜下观察IPC组肺损伤明显减轻。②肺组织湿 /干重比值IPC组为 4.41± 0 .2 4,显著低于I/R组 ,但仍高于缺血前 (P <0 .0 1) ;③IPC组大鼠缺血 1h后MPAP为 ( 1.88± 0 .2 9)kPa ,明显低于I/R组 (P <0 .0 1) ;④IPC组支气管肺泡灌洗液中总磷脂为 ( 2 33 .42± 14.0 5 ) μg/kg ,大聚体为 ( 10 5 .39± 6 .17) μg/kg ,与I/R组相比显著增高 ,但低于对照组 (P <0 .0 1) ,三组之间小聚体含量没有显著差异 ;⑤IPC组表面张力为 ( 36 .88± 3.49)mN/m ,显著低于I/R组 ,与对照组相比则无显著性差异 (P >0 .0 5 )。结论 :缺血预处理对大鼠肺I/R损伤有保护作用 ,保护机制可能与促进肺表面活性物质 (PS)磷脂分泌、改善PS组成 ,从而提高PS功能有关。     

维甲酸X受体介导的氧化应激通路在大鼠肺缺血/再灌注损伤中的调控作用

本研究旨在探讨维甲酸X受体(retinoid X receptor, RXR)介导的氧化应激通路对大鼠肺缺血/再灌注损伤(pulmonary ischemia/reperfusion injury, PIRI)的干预作用及机制。选取雄性Sprague Dawley (SD)大鼠77只,随机分为7组(n=11):正常对照组(Control组)、假手术组(Sham组)、假手术+9-顺式维甲酸(9-cis retinoid acid,9-cRA,RXR激动剂)组(Sham+9-cRA组)、假手术+HX531 (RXR抑制剂)组(Sham+HX531组)、缺血/再灌注(ischemia/reperfusion, I/R)组、I/R+9-cRA组、I/R+HX531组。采用大鼠在体左侧肺门夹闭30 min再灌注180 min方法制备肺缺血/再灌注(I/R)模型。I/R+9-cRA组和I/R+HX531组大鼠于开胸前腹腔注射9-cRA和HX531。再灌注结束后取左肺组织,评估肺组织损伤,用试剂盒检测肺组织氧化应激等相关指标,用HE染色法和透射电镜分别观察肺组织形态和肺泡上皮细胞超微结构,用免疫荧光标记法观察肺组织RXRα的表达情况,用Western blot检测核因子E2相关因子(nuclear factor E2-related factor 2, Nrf2)蛋白表达情况。结果显示,与Sham组相比,I/R组肺组织出现明显损伤,SOD活性下降,MDA含量和MPO活性升高,Nrf2蛋白表达水平显著降低;与I/R组相比,I/R+9-cRA组肺组织损伤减轻,SOD活性升高,MDA含量和MPO活性下降,RXR和Nrf2蛋白表达水平明显上调。9-cRA的上述改善作用可被HX531逆转。上述结果提示,激动RXR可有效减轻大鼠肺I/R损伤,对肺组织有一定的保护作用,具体机制可能与其激活Nrf2信号途径,增强抗氧化水平,减轻氧化应激反应有关。     

大鼠肢体缺血/再灌注后多器官水肿及丹参的预防作用

目的:探讨大鼠肢体缺血/再灌注(LI/R)导致的多器官水肿及丹参的防治作用。方法:Wistar大鼠24只随机分为3组(n=8):对照组(C组)、缺血/再灌注组(I/R组)和丹参预处理组(SM组)。以止血带法制作大鼠肢体缺血/再灌注模型,SM组在再灌注前30 min经尾静脉推注丹参注射液5 ml/kg。准确留取每只动物的心、肝、肾、肺、脑、肠及骨骼肌组织各1 g,恒温烘干后称其干重并计算各组织的湿干重比值(W/D)。采用ELISA法测定血清白细胞介素1(IL-1)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNFα-)含量;采用生物化学方法测定超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量。光镜下观察骨骼肌组织的形态学变化。结果:LI/R后各组织W/D均增加(P<0.05,P<0.01),血浆SOD活性降低而MDA含量增加(P<0.05,P<0.01),血清IL-1、IL-6、TNFα-水平均升高(P<0.05,P<0.01),骨骼肌组织镜下可见炎细胞浸润、肌纤维间隙增宽等病理改变。而SM组与单纯再灌注组比较,血清炎症因子水平下降,氧化损伤程度减轻,镜下组织形态学变化有所改善。结论:大鼠肢体缺血/再灌注可导致多器官水肿,丹参可通过抑制炎症反应、抗氧化等途径在一定程度上预防肢体缺血/再灌注后多器官的水肿。     

金属硫蛋白参与肺缺血预处理的保护作用

本实验旨在探讨金属硫蛋白是否参与肺缺血预处理(ischemic preconditioning,IP)的保护作用。实验用健康雄性Sprague-Dawley大鼠24只,随机分为对照组、肺缺血/再灌注(ischemia-reperfusion,I/R)组和IP组,对比观察各组肺组织中金属硫蛋白(metallothionein,MT)的含量,血清中丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)及髓过氧化物酶(myeloperoxidase,MPO)活性的变化,用原位缺口末端标记法(TUNEL)检测肺组织细胞的凋亡情况,用透射电镜观察肺组织超微结构的改变。结果显示,与对照组相比,I/R组肺组织中MT的含量显著下降(P0.05),血清MDA含量、MPO活性明显升高(P0.01),SOD活性明显下降(P0.01),凋亡指数(apoptosis index,AI)显著增高(P0.01),肺组织超微结构发生异常改变;与I/R组相比,IP组肺组织中MT的含量显著升高(P0.01),血清MDA含量、MPO活性明显下降,SOD活性明显升高(P0.05或P0.01),AI为14.76±1.35,显著低于I/R组(P0.01),肺组织超微结构显著改善。根据以上结果,我们推断诱导MT的产生可能是IP肺保护作用的机制之一。     

Tetanic contraction induces enhancement of fatigability and sarcomeric damage in atrophic skeletal muscle and its underlying molecular mechanisms

Muscle unloading due to long-term exposure of weightlessness or simulated weightlessness causes atrophy, loss of functional capacity, impaired locomotor coordination, and decreased resistance to fatigue in the antigravity muscles of the lower limbs. Besides reducing astronauts＇ mobility in space and on returning to a gravity environment, the molecular mechanisms for the adaptation of skeletal muscle to unloading also play an important medical role in conditions such as disuse and paralysis. The tail-suspended rat model was used to simulate the effects of weightlessness on skeletal muscles and to induce muscle unloading in the rat hindlimb. Our series studies have shown that the maximum of twitch tension and the twitch duration decreased significantly in the atrophic soleus muscles, the maximal tension of high-frequency tetanic contraction was significantly reduced in 2-week unloaded soleus muscles, however, the fatigability of high- frequency tetanic contraction increased after one week of unloading. The maximal isometric tension of intermittent tetanic contraction at optimal stimulating frequency did not alter in 1- and 2-week unloaded soleus, but significantly decreased in 4-week unloaded soleus. The 1-week unloaded soleus, but not extensor digitorum Iongus （EDL）, was more susceptible to fatigue during intermittent tetanic contraction than the synchronous controls. The changes in K＋ channel characteristics may increase the fatigability during high-frequency tetanic contraction in atrophic soleus muscles. High fatigability of intermittent tetanic contraction may be involved in enhanced activity of sarcoplasmic reticulum Ca2＋-ATPase （SERCA） and switching from slow to fast isoform of myosin heavy chain, tropomyosin, troponin I and T subunit in atrophic soleus muscles. Unloaded soleus muscle also showed a decreased protein level of neuronal nitric oxide synthase （nNOS）, and the reduction in nNOS-derived NO increased frequency of calcium sparks and elevated intracellular resting Ca2＋ concentration （[Ca2＋]i） in unloaded soleus muscles. High [Ca2＋]i activated calpain-1 which induced a higher degradation of desmin. Desmin degradation may loose connections between adjacent myofibrils and further misaligned Z-disc during repeated tetanic contractions. Passive stretch in unloaded muscle could preserve the stability of sarcoplasmic reticulum Ca2＋ release channels by means of keeping nNOS activity, and decrease the enhanced protein level and activity of calpain to control levels in unloaded soleus muscles. Therefore, passive stretch restored normal appearance of Z-disc and resisted in part atrophy of unloaded soleus muscles. The above results indicate that enhanced fatigability of high-frequency tetanic contraction is associated to the alteration in K＋ channel characteristics, and elevated SERCA activity and slow to fast transition of myosin heavy chain （MHC） isoforms increases fatigability of intermittent tetanic contraction in atrophic soleus muscle. The sarcomeric damage induced by tetanic contraction can be retarded by stretch in atrophic soleus muscles.     

姜黄素对大鼠脑缺氧缺血损伤时脑组织MDA变化、caspase-3表达及细胞凋亡的影响

目的:探讨姜黄素对大鼠脑缺氧缺血损伤时脑组织MDA变化、caspase-3表达及细胞凋亡的影响。方法:健康SD雄性大鼠48只,随机分为假手术对照组(SH组)、脑缺氧缺血组(HI组)、姜黄素组(CU组)、溶剂对照组(SC组);生化方法检测脑组织丙二醛(MDA)含量;免疫组织化学测定大脑皮质caspase-3的表达;电镜观察大脑皮质形态学结构变化。结果:姜黄素可使脑组织MDA含量明显减低,并且抑制caspase-3蛋白的表达;神经元细胞凋亡减轻。结论:细胞凋亡参与了大脑缺氧缺血损伤的发生,姜黄素可能通过减低MDA含量、下调caspase-3的表达抑制细胞凋亡,从而减轻脑缺氧缺血性损伤。     

Dissecting the Heat Stress Response in Chlamydomonas by Pharmaceutical and RNAi Approaches Reveals Conserved and Novel Aspects

To study how conserved fundamental concepts of the heat stress response （HSR） are in photosynthetic eukaryotes, we applied pharmaceutical and antisense/amiRNA approaches to the unicellular green alga Chlamydomonas reinhardtii. The Chlamydomonas HSR appears to be triggered by the accumulation of unfolded proteins, as it was induced at ambient temperatures by feeding cells with the arginine analog canavanine. The protein kinase inhibitor staurosporine strongly retarded the HSR, demonstrating the importance of phosphorylation during activation of the HSR also in Chlamydomonas. While the removal of extracellular calcium by the application of EGTA and BAPTA inhibited the HSR in moss and higher plants, only the addition of BAPTA, but not of EGTA, retarded the HSR and impaired thermotoler- ance in Chlamydomonas. The addition of cycloheximide, an inhibitor of cytosolic protein synthesis, abolished the attenu- ation of the HSR, indicating that protein synthesis is necessary to restore proteostasis. HSP90 inhibitors induced a stress response when added at ambient conditions and retarded attenuation of the HSR at elevated temperatures. In addition, we detected a direct physical interaction between cytosolic HSP90A/HSP70A and heat shock factor 1, but surprisingly this interaction persisted after the onset of stress. Finally, the expression of antisense constructs targeting chloroplast HSP70B resulted in a delay of the cell＇s entire HSR, thus suggesting the existence of a retrograde stress signaling cascade that is desensitized in HSP7OB-antisense strains.     

Cell Wall,Cytoskeleton, and Cell Expansion in Higher Plants

To accommodate two seemingly contradictory biological roles in plant physiology, providing both the rigid structural support of plant cells and the adjustable elasticity needed for cell expansion, the composition of the plant cell wall has evolved to become an intricate network of cellulosic, hemicellulosic, and pectic polysaccharides and protein. Due to its complexity, many aspects of the cell wall influence plant cell expansion, and many new and insightful observations and technologies are forthcoming. The biosynthesis of cell wall polymers and the roles of the variety of proteins involved in polysaccharide synthesis continue to be characterized. The interactions within the cell wall polymer network and the modification of these interactions provide insight into how the plant cell wall provides its dual function. The complex cell wall architecture is controlled and organized in part by the dynamic intracellular cytoskeleton and by diverse trafficking pathways of the cell wall polymers and cell wall-related machinery. Meanwhile, the cell wall is continually influenced by hormonal and integrity sensing stimuli that are perceived by the cell. These many processes cooperate to construct, maintain, and manipulate the intricate plant cell wall--an essential structure for the sustaining of the plant stature, growth, and life.     

Redox Regulation of Arabidopsis Mitochondrial Citrate Synthase

Citrate synthase has a key role in the tricarboxylic （TCA） cycle of mitochondria of all organisms, as it cata- lyzes the first committed step which is the fusion of a carbon-carbon bond between oxaloacetate and acetyl CoA. The regulation of TCA cycle function is especially important in plants, since mitochondrial activities have to be coordinated with photosynthesis. The posttranslational regulation of TCA cycle activity in plants is thus far almost entirely unexplored. Although several TCA cycle enzymes have been identified as thioredoxin targets in vitro, the existence of any thioredoxin-dependent regulation as known for the Calvin cycle, yet remains to be demonstrated. Here we have investigated the redox regulation of the Arabidopsis citrate synthase enzyme by site-directed mutagenesis of its six cysteine residues. Our results indicate that oxidation inhibits the enzyme activity by the formation of mixed disulfides, as the partially oxidized citrate synthase enzyme forms large redox-dependent aggregates. Furthermore, we were able to demonstrate that thioredoxin can cleave diverse intraas well as intermolecular disulfide bridges, which strongly enhances the activity of the enzyme. Activity measurements with the cysteine variants of the enzyme revealed important cysteine residues affecting total enzyme activity as well as the redox sensitivity of the enzyme.     

Regulation of Cytokinesis by Exocyst Subunit SEC6 and KEULE in Arabidopsis thaliana

Proper vesicle tethering and membrane fusion at the cell plate are essential for cytokinesis. Both the vesicle tethering complex exocyst and membrane fusion regulator KEULE were shown to function in cell plate formation, but the exact mechanisms still remain to be explored. In this study, using yeast two-hybrid （Y-2-H） assay, we found that SEC6 interacted with KEULE, and that a small portion of C-terminal region of KEULE was required for the interaction. The direct SEC6-KEULE interaction was supported by further studies using in vitro pull-down assay, immunoprecipitation, and in vivo bimolecular florescence complementation （BIFC） microscopy, sec6 mutants were male gametophytic lethal as reported; however, pollen-rescued sec6 mutants （PRsec6） displayed cytokinesis defects in the embryonic cells and later in the leaf pavement cells and the guard cells. SEC6 and KEULE proteins were co-localized to the cell plate during cytokine- sis in transgenic Arabidopsis. Furthermore, only SEC6 but not other exocyst subunits located in the cell plate interacted with KEULE in vitro. These results demonstrated that, like KEULE, SEC6 plays a physiological role in cytokinesis, and the SEC6-KEULE interaction may serve as a novel molecular linkage between arriving vesicles and membrane fusion machin- ery or directly regulate membrane fusion during cell plate formation in plants.     

Perturbation of Auxin Homeostasis Caused by Mitochondrial FtSH4 Gene-Mediated Peroxidase Accumulation Regulates Arabiclopsis Architecture

Reactive oxygen species and auxin play important roles in the networks that regulate plant development and morphogenetic changes, However, the molecular mechanisms underlying the interactions between them are poorly understood. This study isolated a mas （More Axillary Shoots） mutant, which was identified as an allele of the mitochondrial AAA-protease AtFtSH4, and characterized the function of the FtSH4 gene in regulating plant development by medi- ating the peroxidase-dependent interplay between hydrogen peroxide （H2Oz） and auxin homeostasis. The phenotypes of dwarfism and increased axillary branches observed in the mas （renamed as ftsh4-4） mutant result from a decrease in the IAA concentration. The expression levels of several auxin signaling genes, including IAA1, IAA2, and IAA3, as well as several auxin binding and transport genes, decreased significantly in ftsh4-4 plants. However, the H202 and peroxidases levels, which also have IAA oxidase activity, were significantly elevated in ftsh4-4 plants. The ftsh4-4 phenotypes could be reversed by expressing the iaaM gene or by knocking down the peroxidase genes PRX34 and PRX33. Both approaches can increase auxin levels in the ftsh4-4 mutant. Taken together, these results provided direct molecular and genetic evidence for the interaction between mitochondrial ATP-dependent protease, H2O2, and auxin homeostasis to regulate plant growth and development.     

Knights in Action： Lectin Receptor-Like Kinases in Plant Development and Stress Responses

The Receptor-Like Kinase （RLK） is a vast protein family with over 600 genes in Arabidopsis and 1100 in rice. The Lectin RLK （LecRLK） family is believed to play crucial roles in saccharide signaling as well as stress perception. All the LecRLKs possess three domains： an N-terminal lectin domain, an intermediate transmembrane domain, and a C-terminal kinase domain. On the basis of lectin domain variability, LecRLKs have been subgrouped into three subclasses： L-, G-, and C-type LecRLKs. While the previous studies on LecRLKs were dedicated to classification, comparative structural analysis and expression analysis by promoter-based studies, most of the recent studies on LecRLKs have laid special emphasis on the potential of this gene family in regulating biotic/abiotic stress and developmental pathways in plants, thus mak- ing the prospects of studying the LecRLK-mediated regulatory mechanism exceptionally promising. In this review, we have described in detail the LecRLK gene family with respect to a historical, evolutionary, and structural point of view. Furthermore, we have laid emphasis on the LecRLKs roles in development, stress conditions, and hormonal response. We have also discussed the exciting research prospects offered by the current knowledge on the LecRLK gene family. The multitude of the LecRLK gene family members and their functional diversity mark these genes as both interesting and worthy candidates for further analysis, especially in the field of crop improvement.