If you are here then it means that you are also just like me, curious and stressed. Curious to know the worldly things and stressed as there is too much in this world. But do our cells or organs also get stressed? Have you ever thought about it?
Therefore, today we will be working to find the answer of this very question. While exploring, we will also find those words or terms that are very simple but deep.
In our normal life routine, not just medical students or physicians, but each and every human have used these words once in their life time. As, each and every human have been themselves or have seen their close ones, with at least one type of disease. Isn’t it?
Therefore, today we will be knowing about:
- Cell adaptations
- Cell injury
Cell injury is caused by anything that our cell is unable to adapt to. Now what in the world this statement means. Well, let’s get into it.
It is interesting to know that our cells have ability to adapt to any change. Actually, it is pretty obvious so it might not be that interesting!
But you might have never put a meaningful thought into it.
Whenever there is any stress put onto a cell, cell within its limits try to adapt to the applied stress to better handle it. If those stresses are up to the limit of cells, it is good for the cell and for us. But ‘if’ the stress gets out of hand, cell gets injured. This is the basic idea of cell injury.
Now, what kind of changes/adaptations do we see?
Cellular changes are either physiological or pathological. Physiological i.e. as per the demand of our life time without any abnormality. Eg, Uterus extension during pregnancy. It is not any kind of injury. It is just the requirement of mother for fetal growth during pregnancy.
Other are pathological changes. Eg, During systemic hypertension, heart gets hypertrophic as myocytes get their size increased. This is called hypertrophy. We will learn about it in just in a while.
Now, this was just the simple differentiation of cellular changes. Next, we will learn about types of adaptations that our cells perform to overcome the stress.
They are as followings:
- Hyperplasia: Hyper means increased and plasia means formation, growth. Thereby, after combining both words we get ‘increased cell proliferation’. This happens as per the demand of the stress. (Q#1)
- Mechanism- Stem cells are stimulated to increase the number of cells. Eg, endometrial hyperplasia.
- One must remember that, adaptations are generally reversible. But if the stress is remains for longer, these can turn either cancerous or can lead to dysplasia.
What is dysplasia? I don’t know about this but do you know that mitochondrion is the powerhouse of the cell.
Just joking. No, not about the mitochondrion being the powerhouse of the cell. This is most common thing that we hear from any biology or non-biology student saying. I was joking about the dysplasia. We will, in the later of this blog, going to learn about this too.
- Hypertrophy: Increase in size of cells and organ.
- Mechanism- Increase of genomic function as it contributes to the formation of newer proteins and organelles for size growth. Eg, Myocardial hypertrophy during systemic hypertension.
- Atrophy: Organ size decreases.
- Mechanism- There are 2 mechanisms of decreasing an organ size i.e. by decreasing cell numbers or cell size itself.
- Cell number reduction- It is achieved simply by apoptosis i.e. programmed cell death. We will learn more about it soon.
- Cell size reduction- It has further 2 mechanisms. One is ubiquitin-proteasome degradation pathway where the cytoskeleton filaments are tagged by ubiquitin -> proteasome recognises it and disintegrates it. Second is autophagy where the vacuoles are formed within the cells containing cellular elements -> fused with lysosomes containing hydrolytic enzymes for decomposition.
- Metaplasia: A type cellular adaptaion when stress is changed. The new cell type is better at adapting to stress.
- Mechanism- Reprogramming of stem cells. Classic example is Barett esophagus.
- In this, the gastric acid reflux creates a newer type of stress for esophagus.
- As we all know, esophagus provides a passage for passing of food from pharynx into stomach. For this, esophagus has surface epithelium made of nonkeratinised stratified squamous epithelium (lubricative and protective against friction).
- In presence of acid, this changes into mucus producing columnar cells (mucus protects against stomach acid that’s why stomach is filled with foveolar cells i.e. mucus producing surface cells).
- This change with the removal of acid gets reversed. Otherwise, consistent stress could even lead to adenocarcinoma (cancer or dysplasia).
Q#1. Do all cells go hyperplasia under stress?
A#1. No. Cells those have permanent growth can’t go hyperplasia. Like- neurons, myocytes of cardiac and skeletal muscles. For these cells, only hypertrophy could be performed.
Other thing is that, for other tissues, generally hyperplasia and hypertrophy goes together.
- Dysplasia: Disorganised growth of cells. These are referred as precancerous cells. Also involves epithelial cells like some previous adaptations.
- Arises from consistent pathological hyperplasia and metaplasia. Examples that we studied earlier i.e. endometrial hyperplasia and barett esophagus respectively.
- Characterised by pleomorphism (A#1).
- Theoretically, it is also reversible but persistent dysplasia can also turn cancerous making it an irreversible change.
These were all the changes that we see cells performing to adapt except the last one as practically it is an undesirable change.
Now moving ahead, let’s talk about cell injury. You may have gotten a fair idea how our cell adapts?
Now we will understand what kind of injuries we are talking about when cells fail to adapt.
There are basically 2 types of injury. One is reversible and other is irreversible. Pretty simple. Now elaborating them…
- Revesible cell injury: As the name says, it is the injury that gets reversed or healed as the stressful condition is removed. It is the initial phase of cellular injury. It occurs when some needy cellular functions are impaired.
- Inability to produce ATP (A#2).
- Reduction in ATP leads to many functional incapability such as cellular pump dysfunction. Eg, Na+/K+ pump leading sodium ion accumulation inside the cell and Ca+ pump leading to influx of calcium ions. Both these leads to cell swelling which is the characteristic and earliest feature of the reversible cell injury.
- Cellular machinery like mitochondria (ATP forming double membrane bean shaped organelles) and endoplasmic reticulum (protein forming double membrane structure) also swells up where in the later this swelling causes ribosome to be detached reducing the protein production.
- Nuclear material like chromatin (A#3) clusters into spherical spaces.
- Plasma membrane forms blebs.
A#1. Pleomorphism: Same cells with different shape, size or any loss of morphological feature.
A#2. Adenosine triphosphate: Just as the mitochondrion is the powerhouse of the cell. ATP is the energy currency of the cell. These are nucleotides (adenosine linked with a ribose sugar) that play the role of energy carrier. They carry energy in the form of bond of its phosphate molecules which on hydrolysis/breakdown gets released.
A#3. Chromatin: It is the beads in thread like structure of genetic material. It is formed by wrapping of nucleic acid (DNA) onto nucleosome (cluster of histone proteins).
Do not confuse it with chromosome. Chromosome has a particular shape formed after further condensation of chromatin.
- Irreversible cell injury: The continuation of reversible injury leads to irreversible injury.
- Mitochondrial membrane gets damaged thereby impairing ATP formation and could lead to apoptosis. (Q#2)
- Plasma membrane destruction leading to release of cellular indicators into serum characterising permanent cell damage. Eg, High level of troponin (A#4) from cardiac muscle damage like heart attack (Q#3). This membrane damage also leads to increased accumulation of Ca+ ions inside the cell. How this is a bad thing? Jump into the next point, I will explain there.
- Lysosomal membrane damage causing its hydrolytic enzymes to leak and digest the cellular components. These enzymes are activated by Ca+ ions which at the moment are already found inside the cytosol. Process after rupturing of lysosomal membrane is called autolysis.
- Occurring of following steps. Pyknosis i.e. irreversible chromatin condensation -> karyorrhexis i.e. chromatin fragmentation -> karyolysis i.e. complete chromatin dissolution.
Q#2. How mitochondrial membrane damage leads to apoptosis?
A#2. Before answering this, I want to say a few words on ATP formation of mitochondrion. You might not know but mitochondrion is the powerhouse of the cell. You knew? I wonder how!
And you also know that mitochondrion is a double membrane organelle. The outer membrane is involved with metabolite and ionic exchange between itself and the cell. The inner membrane is involved with the ATP formation as the components of ETC i.e. electron transport chain are embedded in it. One of the component is Cyt C.
As the membrane gets destroyed, so does the ETC. Also it leads to crossing of Cyt C into cytosol (cytoplasm without cell organelles or simply saying it is the fluid matrix of cytoplasm).
Cyt C is electron carrier from one complex (complex BC1)to another (Cyt C oxidase). (More about it some other time as it itself is a huge topic to cover.)
This protein is also an activator of caspase cascade which regulates the programmed cell death i.e. apoptosis. I will be covering this in the next blog.
Q#3. I have an interesting question. Can you differentiate heart failure with heart attack?
A#3. Heart failure: Here, heart doesn’t pump enough blood as per the body’s need. Think of it as this, heart ‘fails’ to fulfil body’s need.
Heart attack: It is the condition where heart itself doesn’t get enough blood as per its need. It’s like attack on heart itself where it gets damaged. Also known as by myocardial infarction. Myocardial means the muscular layer of heart and infarction means tissue death after obstruction of blood supply to a certain part. And now don’t confuse it with ischemia. Ischemia is reduction in blood flow through an organ.
A#4. Troponin: It is a group of protein found in contractile cells. It’s role is to help in contraction of the muscle.
I feel like this time, the topic was very easy. I guess it’s not a bad thing. Though, even if it is easy, it is enough to let you answer some interesting and important questions.
After going through all this, you can answer:
- How cell adapts?
- What can happen if they fail to adapt?
- Types of adaptations
- What happens when cellular injury is temporary?
- What happens when cellular injury is permanent?
- Basic idea of apoptosis etc.
I have made this list of important questions that could be answered by reading this blog. You can give it a try. If you are unable to answer, then you may read it again. If still you have any query, just comment below.
I hope you have liked it. Next blog will be a continuation to this one.